Biological and Non-Biological Therapy in Pemphigus: An Updated Therapeutic Guide

Andrés Tirado-Sánchez
Department of Dermatology, Hospital General de Mexico and Instituto Mexicano del Seguro Social, Mexico

Series: Dermatology – Laboratory and Clinical Research
BISAC: SCI013040



Volume 10

Issue 1

Volume 2

Volume 3

Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick


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The main objective in treating pemphigus vulgaris is to control the disease, prevent relapses, and avoid adverse events associated with the prolonged use of steroids and immunosuppressive agents. Finding the most effective steroid-sparing agent has formed much of the focus of recent research. Systemic corticosteroids remain the gold standard for pemphigus vulgaris. In this book, the reader will have a complete view of this group of life-threatening diseases through direct images, tables and text. This book is not only of interest to dermatologists, but for all those health professionals whom at some point in their lives have tried or at least had the opportunity to see a patient with these diseases. This book is obviously also intended for those who have experienced first hand pemphigus vulgaris. This book is also a suitable medium for understanding the pemphigus group. Residents and researchers in dermatology and close disciplines can use the book as a quick reference guide when dealing with these patients.

This book will help both dermatologists and non-dermatology physicians for treating each disease practically. Each chapter reviews the current literature of treatments for each disease, rates disease severity, and provides guidelines for the use of available medications. This book will help guide clinicians in carrying out suitable treatments based on the severity. The author aims to provide a quick study guide for students and a reference for physicians who practice treating these types of patients. The author hopes the reader enjoys reading this book as much as he did composing it. (Imprint: Nova Biomedical)

Part 1. Physiological and Pathological Backround

Chapter 1. The Biology of the Epidermis. The Basics.

Chapter 2. The Immune System in Normal Skin and in Pemphigus Skin

Part 2. Ethiopathogenesis of Pemphigus

Chapter 3. Desmosomal Protein Targets in Pemphigus

Chapter 4. Apoptosis and Acantholysis in Pemphigus. The Concept of Apoptolysis

Chapter 5. Genetic and Environmental Risk Factors of Pemphigus

Part 3. Epidemiology

Chapter 6. Epidemiology of Pemphigus

Part 4. Clinical Presentation of Pemphigus

Chapter 7. Clinical Presentation of Pemphigus Vulgaris

Chapter 8. Clinical Presentation of Pemphigus Foliaceus

Chapter 9. Paraneoplastic Pemphigus

Chapter 10. IgA Pemphigus

Part 5. Diagnostic Tests

Chapter 11. Diagnosis of Pemphigus

Chapter 12. ELISA Test and Immunoblotting

Chapter 13. Electron Microscopy and Immunoelectron Microscopy

Part 6. General Management of Pemphigus

Chapter 14. Non-biological Therapy

Chapter 15. Biological Therapy

Part 7. Detailed Management of Pemphigus. Non-Biological Therapy

Chapter 16. Costicosteroids

Chapter 17. Treatment and Prevention of Glucocorticoid-Induced Osteoporosis

Chapter 18. Prevention and Therapy of Steroid-Induced Diabetes

Chapter 19. Prevention and Treatment of Infections

Chapter 20. Azathioprine

Chapter 21. Mycophenolate Mofetil/Mycophenolic Acid

Chapter 22. Dapsone

Chapter 23. Cyclophosphamide

Chapter 24. Tetracyclines

Part 7. Specific Management of Pemphigus. Biological Therapy

Chapter 25. Intravenous Immunoglobulins

Chapter 26. Rituximab

Chapter 27. Etanercept and Other Anti-TNF

Part 8. Additional Therapy and Monitoring

Chapter 28. Management of Pain in Pemphigus Vulgaris

Chapter 29. Extent Measures in Pemphigus

Chapter 30. Quality of Life in Pemphigus


[1] Müller, EJ; Galichet, A; Wiener, D; et al. Keratinocyte biology and pathology. Vet Dermatol, 2014, 25, 236-8.
[2] Nishifuji, K; Yoon, JS. The stratum corneum: the rampart of the mammalian body. Vet Dermatol, 2013, 24, 60–72.
[3] Suter, MM; Schulze, K; Bergman, W; et al. The keratinocyte in epidermal renewal and defence. Vet Dermatol, 2009, 20, 515–32.
[4] Drögemüller, M; Jagannathan, V; Becker, D; et al. A mutation in the FAM83G gene in dogs with hereditary footpad hyperkeratosis (HFH). PLoS Genet, 2014, 10, e1004370.
[5] Jagannathan, V; Bannoehr, J; Plattet, P; et al. A mutation in the SUV39H2 gene in Labrador Retrievers with hereditary nasalparakeratosis (HNPK) provides insights into the epigenetics of keratinocyte differentiation. PLoS Genet, 2013, 9, e1003848.
[6] Müller, EJ; Caldelari, R; Kolly, C; et al. Consequences of depleted SERCA2-gated calcium stores in the skin. J Invest Dermatol, 2006, 126, 721–31.
[7] Klukowska-Rötzler, J; Chervet, L; Müller, EJ; et al. Expression of thymicstromal lymphopoiet in in canine atopic dermatitis. Vet Dermatol, 2013, 24, 54–9.
[8] Chervet, L; Galichet, A; McLean, WH; et al. Missing C-terminal filaggrin expression, NFkappaB activation and hyperproliferation identify the dog as a putative model to study epidermal dysfunction in atopic dermatitis. Exp Dermatol, 2010, 19, e343–e346.
[9] Owczarek-Lipska, M; Lauber, B; Molitor, V; et al. Two loci on chromosome 5 are associated with serum IgE levels in Labrador retrievers. PLoS One, 2012, 7, e39176.
[10] Lauber, B; Molitor, V; Meury, S; et al. Total IgE and allergen-specific IgE and IgG antibody levels in sera of atopic dermatitis affected and non-affected Labrador- and Golden retrievers. Vet Immunol Immunopathol, 2012, 149, 112–118.
[11] Williamson, L; Raess, NA; Caldelari, R; et al. Pemphigus vulgaris identifies plakoglobin as key suppressor of c-Myc in the skin. EMBO J, 2006, 25(14), 3298–309.
[12] Muller, EJ; Williamson, L; Kolly, C; Suter, MM. Outside-in signaling through integrins and cadherins, a central mechanism to control epidermal growth and differentiation? J Invest Dermatol, 2008, 128(3), 501–16.
[13] Galichet, A; Borradori, L; Müller, EJ. A new light on an old disease: adhesion signaling in pemphigus vulgaris. J Invest Dermatol, 2014, 134, 8–10.
[14] Getsios, S; Waschke, J; Borradori, L; et al. From cell signaling to novel therapeutic concepts: international pemphigus meeting on advances in pemphigus research and therapy. J Invest Dermatol, 2010, 130, 1764–8.
[15] Blanpain, C; Horsley, V; Fuchs, E. Epithelial stem cells: turning over new leaves. Cell, 2007, 128, 445–58.
[16] Kolly, C; Suter, MM; Müller, EJ. Proliferation, cell cycle exit, and onset of terminal differentiation in cultured keratinocytes: pre-programmed pathways in control of C-Myc and Notch1 prevailover extracellular calcium signals. J Invest Dermatol, 2005, 124, 1014–25.
[17] Caldelari, R; Müller, EJ. Short- and long-term cultivation of embryonic and neonatal murine keratinocytes. Methods Mol Biol, 2010, 633, 125–38.
[18] Sasai, Y. Cytosystems dynamics in self-organization of tissue architecture. Nature, 2013, 493, 318–26.
[19] Bos, JD; Kapsenberg, ML. The skin immune system: progress in cutaneous biology. Immunol Today, 1993, 14(2), 75–8.
[20] Streilein, JW. Skin-associated lymphoid tissues (SALT): origins and functions. J Invest Dermatol, 1983, 80(Suppl), 12–6.
[21] Egawa, G; Kabashima, K. Skin as a peripheral lymphoid organ: revisiting the concept of skin- associated lymphoid tissues. J Invest Dermatol, 2011, 131(11), 2178–85.
[22] Nestle, FO; Di Meglio, P; Qin, JZ; Nickoloff, BJ. Skin immune sentinels in health and disease. Nat Rev Immunol, 2009, 9(10), 679–91.
[23] Gorelik, M; Frischmeyer-Guerrerio, PA. Innate and adaptive dendritic cell responses to immunotherapy. Curr Opin Allergy Clin Immunol, 2015, 15(6), 575-80.
[24] Schakel, K; Hansel, A. News from dendritic cells in atopic dermatitis. Curr Opin Allergy Clin Immunol., 2011, 11(5), 445–50.
[25] Di Meglio, P; Perera, GK; Nestle, FO. The multitasking organ: recent insights into skin immune function. Immunity, 2011, 35(6), 857–69.
[26] Tomura, M; Honda, T; Tanizaki, H; et al. Activated regulatory T cells are the major T cell type emigrating from the skin during a cutaneous immune response in mice. J Clin Invest, 2010, 120(3), 883–93.
[27] Machado, I; González, P; Schiöth, HB; Lasaga, M; Scimonelli, TN. α-Melanocyte-stimulating hormone (α-MSH) reverses impairment of memory reconsolidation induced by interleukin-1 beta (IL-1 beta) hippocampal infusions. Peptides, 2010, 31(11), 2141-4.
[28] Piskin, G; Sylva-Steenland, RMR; Bos, JD; et al. In vitro and in vivo expression of IL-23 by keratinocytes in healthy skin and psoriasis lesions: enhanced expression in psoriatic skin. J Immunol, 2006, 176, 1908–15.
[29] Soumelis, V; Reche, PA; Kanzler, H; et al. Human epithelial cells trigger dendritic cell-mediated allergic inflammation by producing TSLP. Nat Immunol, 2002, 3, 673–80.
[30] Akira, S; Uematsu, S; Takeuchi, O. Pathogen recognition and innate immunity. Cell, 2006, 124, 783–801.
[31] Ting, JPY; Kastner, DL; Hoffman, HM. Caterpillers, pyrin and hereditary immunological disorders. Nat Rev Immunol, 2006, 6, 183–95.
[32] Robinson, MJ; Sancho, D; Slack, EC; et al. Myeloid C-type lectins in innate immunity. Nat Immunol, 2006, 12, 1258–65.
[33] van der Aar, AMG; Sylva-Steenland, RMR; Bos, JD; et al. Cutting edge: loss of TLR2, TLR4, and TLR5 on Langerhans cells abolishes bacterial recognition. J Immunol, 2007, 178, 1986–900.
[34] Medzhitov, R; Janeway, CA. Innate immunity. N Engl J Med, 2000, 343, 338–44.
[35] Esche, C; Stellato, C; Beck, LA. Chemokines: key players in innate and adaptive immunity. J Invest Dermatol, 2005, 125, 615–28.
[36] McGirt, LY; Beck, LA. Innate immune defects in atopic dermatitis. J Allergy Clin Immunol, 2006, 118, 202–8.
[37] Bos, JD; De Rie, MA; Teunissen, MBM; et al. Psoriasis: activation of innate immunity. Br J Dermatol, 2005, 152, 1098–107.
[38] Mihai, S; Sitaru, C. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J Cell Mol Med, 2007, 11(3), 462–81.
[39] Amagai, M; Stanley, JR. Desmoglein as a target in skin disease and beyond. J Invest Dermatol, 2012, 132(3 Pt 2), 776–84.
[40] Tsuruta, D; Dainichi, T; Hamada, T; Ishii, N; Hashimoto, T. Molecular diagnosis of autoimmune blistering diseases. Methods Mol Biol, 2013, 961, 17–32.
[41] Kneisel, A; Hertl, M. Autoimmune bullous skin diseases. Part 1: clinical manifestations. J Dtsch Dermatol Ges, 2011, 9(10), 844–56.
[42] Kneisel, A; Hertl, M. Autoimmune bullous skin diseases. Part 2: diagnosis and therapy. J Dtsch Dermatol Ges, 2011, 9(11), 927–47.
[43] Amagai, M; Matsuyoshi, N; Wang, ZH; Andl, C; Stanley, JR. Toxin in bullous impetigo and staphylococcalscalded-skin syndrome targets desmoglein 1. Nat Med, 2000, 6(11), 1275–7.
[44] Sitaru, C; Mihai, S; Otto, C; et al. Induction of dermal-epidermal separation in mice by passive transfer of antibodies specific to type VII collagen. J Clin Invest, 2005, 115(4), 870–8.
[45] Nishie, W; Sawamura, D; Goto, M; et al. Humanization of autoantigen. Nat Med, 2007, 13(3), 378–83.
[46] Eming, R; Hennerici, T; Backlund, J; et al. Pathogenic IgG antibodies against desmoglein 3 in pemphigus vulgaris are regulated by HLA-DRB1*04: 02-restricted T cells. J Immunol, 2014, 193(9), 4391–9.
[47] Anhalt, GJ; Labib, RS; Voorhees, JJ; Beals, TF; Diaz, LA. Induction of pemphigus in neonatal mice by passive transfer of IgG from patients with the disease. N Engl J Med, 1982, 306(20), 1189–96.
[48] Gushi, M; Yamamoto, Y; Mine, Y; et al. Neonatal pemphigus vulgaris. J Dermatol, 2008, 35(8), 529–35.
[49] Grando, SA. Pemphigus autoimmunity: hypotheses and realities. Autoimmunity, 2012, 45(1), 7–35.
[50] Cirillo, N; Cozzani, E; Carrozzo, M; Grando, SA. Urban legends: pemphigus vulgaris. Oral Dis, 2012, 18(5), 442–58.
[51] Marchenko, S; Chernyavsky, AI; Arredondo, J; Gindi, V; Grando, SA. Antimitochondrial autoantibodies in pemphigus vulgaris: a missing link in disease pathophysiology. J Biol Chem, 2010, 285(6), 3695–704.
[52] Hacker, MK; Janson, M; Fairley, JA; Lin, MS. Isotypes and antigenic profiles of pemphigus foliaceus and pemphigus vulgaris autoantibodies. Clin Immunol, 2002, 105(1), 64–74.
[53] Funakoshi, T; Lunardon, L; Ellebrecht, CT; Nagler, AR; O’Leary, CE; Payne, AS. Enrichment of total serum IgG4 in patients with pemphigus. Br J Dermatol, 2012, 167(6), 1245–53.
[54] Amagai, M; Ahmed, AR; Kitajima, Y; et al. Are desmoglein autoantibodies essential for the immunopathogenesis of pemphigus vulgaris, or just “witnesses of disease”? Exp Dermatol, 2006, 15(10), 815–31.
[55] Saito, M; Stahley, SN; Caughman, CY; et al. Signaling dependent and independent mechanisms in pemphigus vulgaris blister formation. PLoS One, 2012, 7(12), e50696.
[56] Yamamoto, Y; Aoyama, Y; Shu, E; Tsunoda, K; Amagai, M; Kitajima, Y. Anti-desmoglein 3 (Dsg3) monoclonal antibodies deplete desmosomes of Dsg3 and differ in their Dsg3-depleting activities related to pathogenicity. J Biol Chem, 2007, 282(24), 17866–76.
[57] Bektas, M; Runager, K; Petersen, JS; Rubenstein, DS. Advances in pemphigus research, signaling, and acantholysis. G Ital Dermatol Venereol, 2010, 145(5), 675–87.
[58] Lotti, R; Marconi, A; Pincelli, C. Apoptotic pathways in the pathogenesis of pemphigus: targets for new therapies. Curr Pharm Biotechnol, 2012, 13(10), 1877–81.
[59] van der Wier, G; Jonkman, MF; Pas, HH; Diercks, GF. Ultrastructure of acantholysis in pemphigus foliaceus re-examined from the current perspective. Br J Dermatol, 2012, 167(6), 1265–71.
[60] Mahoney, MG; Wang, Z; Rothenberger, K; Koch, PJ; Amagai, M; Stanley, JR. Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris. J Clin Invest, 1999, 103(4), 461–8.
[61] Tsuruta, D; Ishii, M; Hashimoto, T. The diagnosis and treatment of pemphigus. Immunotherapy, 2012, 4(7), 735–45.
[62] Murell, D Ed. Blistering diseases. Springer Ed. Berlin, 2015. ISBN 978-3-662-45697-2.
[63] Serrano-Osuna, R; López-López, RM; Brito-Zurita, OR; Sabag-Ruiz, E; Pérez-Fernández, H; Ornelas-Aguirre, JM. Seroprevalence of antinuclear antibodies in blood donors in the Yaqui Valley. Cir Cir, 2014, 82(6), 619-27.
[64] Kretz-Rommel, A; Rubin, RL. Disruption of positive selection of thymocytes causes autoimmunity. Nat Med, 2000, 6, 298–305.
[65] Stockinger, B. T lymphocyte tolerance: from thymic deletion to peripheral control mechanisms. Adv Immunol, 1999, 71, 229–65.
[66] Bouneaud, C; Kourilsky, P; Bousso, P. Impact of Negative Selection on the T Cell RepertoireReactive to a Self-Peptide. A Large Fraction of T Cell Clones Escapes Clonal Deletion. Immunity, 2000, 13, 829–840.
[67] Kisielow, P; Teh, HS; Bluthmann, H; von Boehmer, H. Positive selection of antigen specific T cells in thymus by restricting MHC molecules. Nature 1988, 335, 730–733.
[68] Rocha, B; von Boehmer, H. Peripheral selection of the T cell repertoire. Science, 1991, 251, 1225–1228.
[69] Leventhal, J; Miller, J; Abecassis, M; Tollerud, DJ; Ildstad, ST. Evolving approaches of hematopoietic stem cell-based therapies to induce tolerance to organ transplants: the long road to tolerance. Clin Pharmacol Ther, 2013, 93(1), 36-45.
[70] Blackman, M; Kappler, J; Marrack, P. The role of the T cell receptor in positive andnegative selection of developing T cells. Science, 1990, 248, 1335–41.
[71] Bonomo, A; Matzinger, P. Thymus epithelium induces tissue-specific tolerance. J Exp Med, 1993, 177, 1153–64.
[72] Arnold, B; Schonrich, G; Hammerling, GJ. Multiple levels of peripheral tolerance. Immunol Today, 1993, 14, 12–4.
[73] Rocken, M; Shevach, EM. Immune deviation – the third dimension of non deletional T cell tolerance. Immunol Rev, 1996, 149, 175–94.
[74] Moskophidis, D; Lechner, F; Pircher, H; Zinkernagel, RM. Virus persistence inacutely infected immunocompetent mice by exhaustion of antiviral cytotoxic effector T cells. Nature, 1993, 362, 758–61.
[75] Webb, S; Morris, C; Sprent, J. Extrathymic tolerance of mature T cells: clonal elimination as a consequence of immunity. Cell, 1990, 63, 1249–56.
[76] Alferink, J; Tafuri, A; Vestweber, D; Hallmann, R; Hammerling, GJ; Arnold, B. Control of neonatal tolerance to tissue antigens by peripheral T cell trafficking. Science, 1998, 282, 1338–41.
[77] Schonrich, G; Kalinke, U; Momburg, F; et al. Down-regulation of T cell receptors on self-reactiveT cells as a novel mechanism for extrathymic tolerance induction. Cell, 1991, 65, 293–304.
[78] Ohashi, PS; Oehen, S; Buerki, K; et al. Ablation of “tolerance” and induction of diabetes by virusinfection in viral antigen transgenic mice. Cell, 1991, 65, 305–17.
[79] Oldstone, MB; Nerenberg, M; Southern, P; Price, J; Lewicki, H. Virus infection triggersinsulin-dependent diabetes mellitus in a transgenic model: role of anti-self (virus) immuneresponse. Cell, 1991, 65, 319–31.
[80] von Herrath, MG; Guerder, S; Lewicki, H; Flavell, RA; Oldstone, MB. Coexpression of B7-1 and viral (“self”) transgenes in pancreatic beta cells can break peripheral ignorance and lead to spontaneous autoimmune diabetes. Immunity, 1995, 3, 727–38.
[81] Weinberg, AD; English, M; Swain, SL. Distinct regulation of lymphokine production is found in fresh versus in vitro primed murine helper T cells. J Immunol, 1990, 144, 1800–7.
[82] Mosmann, TR; Sad, S. The expanding universe of T-cell subsets: Th1, Th2 and more. Immunol Today, 1996, 17, 138–46.
[83] Rocken, M; Racke, M; Shevach, EM. IL-4-induced immune deviation as antigen specific therapy for inflammatory autoimmune disease. Immunol Today, 1996, 17, 225–31.
[84] Rocken, M; Saurat, JH; Hauser, C. A common precursor for CD4+ T cells producingIL-2 or IL-4. J Immunol, 1992, 148, 1031–6.
[85] Adorini, L; Sinigaglia, F. Pathogenesis and immunotherapy of autoimmune diseases. Immunol Today, 1997, 18, 209–11.
[86] Katz, JD; Benoist, C; Mathis, D. T helper cell subsets in insulin-dependent diabetes. Science, 1995, 268, 1185–8.
[87] Kolb, H; Kolb-Bachofen, V; Roep, BO. Autoimmune versus inflammatory type Idiabetes: a controversy? Immunol Today, 1995, 16, 170–2.
[88] Powrie, F. T cells in inflammatory bowel disease: protective and pathogenic roles. Immunity, 1995, 3, 171–4.
[89] Racke, MK; Bonomo, A; Scott, DE; et al. Cytokine-induced immune deviation as a therapy for inflammatory autoimmunedisease. J Exp Med, 1994, 180, 1961–6.
[90] Budinger, L; Borradori, L; Yee, C; et al. Identification and characterization of autoreactive T cell responses tobullous pemphigoid antigen 2 in patients and healthy controls. J Clin Invest, 1998, 102, 2082–9.
[91] Mosmann, TR. Coffman RL. TH1 and TH2 cells: different patterns of lymphokinesecretion lead to different functional properties. Annu Rev Immunol, 1989, 7, 145–73.
[92] Goldman, M; Druet, P; Gleichmann, E. TH2 cells in systemic autoimmunity: insightsfrom allogeneic diseases and chemically-induced autoimmunity. Immunol Today, 1991, 12, 223–7.
[93] Hertl, M; Karr, RW; Amagai, M; Katz, SI. Heterogeneous MHC II restriction pattern of autoreactive desmoglein 3 specific T cell responses in pemphigus vulgarispatients and normals. J Invest Dermatol, 1998, 110(4), 388–92.
[94] Biedermann, T; Zimmermann, S; Himmelrich, H; et al. IL-4 instructs TH1 responses and resistance to Leishmania major in susceptible BALB/c mice. Nat Immunol, 2001, 2, 1054–60.
[95] Ghoreschi, K; Thomas, P; Breit, S; et al. Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease. Nat Med, 2003, 9, 40–6.
[96] Luger, D; Silver, PB; Tang, J; et al. Either a Th17 or a Th1 effector response can drive autoimmunity: conditions of disease induction affect dominant effector category. J Exp Med, 2008, 205, 799–810.
[97] Nestle, FO; Kaplan, DH; Barker, J. Psoriasis. N Engl J Med, 2009, 361, 496–509.
[98] Akdis, CA; Joss, A; Akdis, M; Faith, A; Blaser, K. A molecular basis for T cell suppression by IL-10, CD28-associated IL-10 receptor inhibits CD28 tyrosine phosphorylation and phosphatidylinositol 3-kinase binding. Faseb J, 2000, 14, 1666–8.
[99] Groux, H; O’Garra, A; Bigler, M; et al. A CD4+ T-cell subset inhibits antigen-specific T-cell responses and prevents colitis. Nature, 1997, 389, 737–42.
[100] Bluestone, JA; Tang, Q. Therapeutic vaccination using CD4+CD25+ antigen-specific regulatory T cells. Proc Natl Acad Sci U S A, 2004, 101 Suppl 2, 14622-6.
[101] Walker, MR; Kasprowicz, DJ; Gersuk, VH; et al. Induction of FoxP3 and acquisition of T regulatory activity by stimulatedhuman CD4+CD25- T cells. J Clin Invest, 2003, 112, 1437–1443.
[102] Fontenot, JD; Gavin, MA; Rudensky, AY. Foxp3 programs the development and function of CD4+CD25+ regulatory T cells. Nat Immunol, 2003, 4, 330–6.
[103] Kriegel, MA; Lohmann, T; Gabler, C; Blank, N; Kalden, JR; Lorenz, HM. Defective suppressor function of human CD4+ CD25+ regulatory T cells in autoimmune polyglandular syndrome type II. J Exp Med, 2004, 199, 1285–91.
[104] Xing, Y; Hogquist, KA. T-cell tolerance: central and peripheral. Cold Spring Harb Perspect Biol, 2012, 4(6), 1–15.
[105] Guerder, S; Picarella, DE; Linsley, PS; Flavell, RA. Costimulator B7-1 confers antigen-presenting cell function to parenchymal tissue and in conjunction with tumor necrosis factor alpha leads to autoimmunity in transgenic mice. Proc Natl Acad Sci U S A, 1994, 91, 5138–42.
[106] Sakaguchi, S; Sakaguchi, N; Asano, M; Itoh, M; Toda, M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J Immunol, 1995, 155, 1151–64.
[107] Sakaguchi, S; Takahashi, T; Nishizuka, Y. Study on cellular events in post-thymectomy autoimmune oophoritis in mice. II. Requirement of Lyt-1 cells in normal female mice for the prevention of oophoritis. J Exp Med, 1982, 156, 1577–86.
[108] Smith, H; Sakamoto, Y; Kasai, K; Tung, KS. Effector and regulatory cells in autoimmune oophoritis elicited by neonatal thymectomy. J Immunol, 1991, 147, 2928–33.
[109] Suri-Payer, E; Amar, AZ; Thornton, AM; Shevach, EM. CD4+CD25+ T cells inhibit both the induction and effector function of autoreactive T cells and represent a unique lineage of immunoregulatory cells. J Immunol, 1998, 160, 1212–8.
[110] Chatila, TA; Blaeser, F; Ho, N; Lederman, HM; Voulgaropoulos, C; Helms, C; Bowcock, AM. JM2, encoding a fork head-related protein, is mutated in X-linked autoimmunity-allergic disregulation syndrome. J Clin Invest, 2000, 106, R75–81.
[111] Brunkow, ME; Jeffery, EW; Hjerrild, KA; et al. Disruption of a new forkhead/winged-helix protein, scurfin, results in the fatal lymphoproliferative disorder of the scurfy mouse. Nat Genet, 2001, 27, 68–73.
[112] Fontenot, JD; Rasmussen, JP; Williams, LM; Dooley, JL; Farr, AG; Rudensky, AY. Regulatory T cell lineage specification by the forkhead transcription factor foxp3. Immunity, 2005, 22, 329–41.
[113] Hori, S; Nomura, T; Sakaguchi, S. Control of regulatory T cell development by the transcription factor Foxp3. Science, 2003, 299, 1057–61.
[114] Khattri, R; Cox, T; Yasayko, SA; Ramsdell, F. An essential role for Scurfin in CD4+CD25+ T regulatory cells. Nat Immunol, 2003, 4, 337–42.
[115] Wan, YY; Flavell, RA. Identifying Foxp3-expressing suppressor T cells with a bicistronic reporter. Proc Natl Acad Sci U S A, 2005, 102, 5126–31.
[116] Wing, JB; Sakaguchi, S. Multiple treg suppressive modules and their adaptability. Front Immunol, 2012, 3, 178.
[117] Shevach, EM. Mechanisms of foxp3+ T regulatory cell-mediated suppression. Immunity, 2009, 30, 636–45.
[118] Yamaguchi, T; Wing, JB; Sakaguchi, S. Two modes of immune suppression by Foxp3(+) regulatory T cells under inflammatory or non-inflammatory conditions. Semin Immunol, 2011, 23, 424–30.
[119] Takahashi, T; Tagami, T; Yamazaki, S; et al. Immunologic self-tolerance maintained by CD25(+)CD4(+) regulatory T cells constitutively expressing cytotoxic T lymphocyte-associated antigen 4. J Exp Med, 2000, 192, 303–10.
[120] Tang, Q; Henriksen, KJ; Bi, M; et al. In vitro-expanded antigen-specific regulatory T cells suppress autoimmune diabetes. J Exp Med, 2004, 199, 1455–65.
[121] Tarbell, KV; Yamazaki, S; Olson, K; Toy, P; Steinman, RM. CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppresses autoimmune diabetes. J Exp Med, 2004, 199, 1467–77.
[122] Chen, Z; Herman, AE; Matos, M; Mathis, D; Benoist, C. Where CD4+CD25+ T reg cells impinge on autoimmune diabetes. J Exp Med, 2005, 202, 1387–97.
[123] Atarashi, K; Tanoue, T; Shima, T; et al. Induction of colonic regulatory T cells by indigenous Clostridium species. Science, 2011, 331, 337–41.
[124] Di Ianni, M; Falzetti, F; Carotti, A; et al. Tregs prevent GVHD and promote immune reconstitution in HLA-haploidentical transplantation. Blood, 2011, 117, 3921–8.
[125] Lathrop, SK; Bloom, SM; Rao, SM; et al. Peripheral education of the immune system by colonic commensal microbiota. Nature, 2011, 478, 250–4.
[126] Sagoo, P; Lombardi, G; Lechler, RI. Relevance of regulatory T cell promotion of donor-specific tolerance in solid organ transplantation. Front Immunol, 2012, 3, 184.
[127] Geiger, TL; Tauro, S. Nature and nurture in Foxp3(+) regulatory T cell development, stability, and function. Hum Immunol, 2012, 73, 232–9.
[128] Apostolou, I; von Boehmer, H. In vivo instruction of suppressor commitment in naive T cells. J Exp Med, 2004, 199, 1401–8.
[129] Kretschmer, K; Apostolou, I; Hawiger, D; Khazaie, K; Nussenzweig, MC; von Boehmer, H. Inducing and expanding regulatory T cell populations by foreign antigen. Nat Immunol, 2005, 6, 1219–27.
[130] Haribhai, D; Williams, JB; Jia, S; et al. A requisite role for induced regulatory T cells in tolerance based on expanding antigen receptor diversity. Immunity, 2011, 35, 109–22.
[131] Daniel, BS; Murrell, DF. The actual management of pemphigus. G Ital Dermatol Venerol, 2010, 145, 689–702.
[132] Chen, W; Jin, W; Hardegen, N; Lei, KJ; Li, L; Marinos, N; McGrady, G; Wahl, SM. Conversion of peripheral CD4+CD25- naive T cells to CD4+CD25+ regulatory T cells by TGF-beta induction of transcription factor Foxp3. J Exp Med, 2003, 198, 1875–86.
[133] Peng, Y; Laouar, Y; Li, MO; Green, EA; Flavell, RA. TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. Proc Natl Acad Sci U S A, 2004, 101, 4572–7.
[134] Banchereau, J; Steinman, RM. Dendritic cells and the control of immunity. Nature, 1998, 392, 245–52.
[135] Schuler, G; Steinman, RM. Dendritic cells as adjuvants for immune-mediated resistance to tumors. J Exp Med, 1997, 186, 1183–7.
[136] Schuler, G; Thurner, B; Romani, N. Dendritic cells: from ignored cells to major playersin T-cell-mediated immunity. Int Arch Allergy Immunol, 1997, 112, 317–22.
[137] Chung, CY; Ysebaert, D; Berneman, ZN; Cools, N. Dendritic cells: cellular mediators for immunological tolerance. Clin Dev Immunol, 2013, 2013, 972865.
[138] Kalinski, P; Hilkens, CM; Wierenga, EA; Kapsenberg, ML. T-cell priming by type-1 and type-2 polarized dendritic cells, the concept of a third signal. Immunol Today, 1999, 20, 561–567.
[139] Moser, M; Murphy, KM. Dendritic cell regulation of TH1-TH2 development. Nat Immunol, 2000, 1, 199–205.
[140] Korn, T; Bettelli, E; Oukka, M; Kuchroo, VK. IL-17 and Th17 Cells. Annu Rev Immunol, 2009, 27, 485–517.
[141] Abraham, C; Cho, JH. IL-23 and Autoimmunity: New Insights into the Pathogenesis of Inflammatory Bowel Disease. Annu Rev Med, 2009, 60, 97–110.
[142] Jonuleit, H; Schmitt, E; Schuler, G; Knop, J; Enk, AH. Induction of interleukin10-producing, nonproliferating CD4(+) T cells with regulatory properties by repetitive stimulationwith allogeneic immature human dendritic cells. J Exp Med, 2000, 192, 1213–22.
[143] Volz, T; Nega, M; Buschmann, J; et al. Natural Staphylococcus aureus-derived peptidoglycan fragments activate NOD2 and act as potent costimulators of the innate immune system exclusively in the presence of TLR signals. FASEB J, 2010, 24(10), 4089-102.
[144] Koch, KN; Hartung, ML; Urban, S; et al. Helicobacter urease-induced activation of the TLR2/NLRP3/IL-18 axis protects against asthma. J Clin Invest, 2015, 125(8), 3297-302.
[145] Iwasaki, A; Medzhitov, R. Regulation of Adaptive Immunity by the Innate Immune System. Science, 2010, 5963, 291–5.
[146] Schroder, K; Tschopp, J. The inflammasomes. Cell, 2009, 140, 821–32.
[147] Nagata, S; Hanayama, R; Kawane, K. Autoimmunity and the clearance of dead cells. Cell, 2010, 140, 619–30.
[148] Mocikat, R; Braumuller, H; Gumy, A; et al. Natural killer cells activatedby MHC class I(low) targets prime dendritic cells to induce protective CD8 T cell responses. Immunity, 2003, 19, 561–9.
[149] Rocken, M; Urban, JF; Shevach, EM. Infection breaks T-cell tolerance. Nature, 1992, 359, 79–82.
[150] Harrison, LC; Honeyman, MC; De Aizpurua, HJ; et al. Inverse relation between humoral and cellular immunity to glutamicacid decarboxylase in subjects at risk of insulin-dependent diabetes. Lancet, 1993, 341, 1365–9.
[151] Albert, ML; Sauter, B; Bhardwaj, N. Dendritic cells acquire antigen from apoptotic cells and induce class I-restricted CTLs. Nature, 1998, 392, 86–9.
[152] Matzinger, P; Anderson, CC. Immunity or tolerance: Opposite outcomes of microchimerism from skin grafts. Nat Med, 2001, 7, 80–7.
[153] Naucler, CS; Larsson, S; Moller, E. A novel mechanism for virus-induced autoimmunity in humans. Immunol Rev, 1996, 152, 175–92.
[154] Matzinger, P. Tolerance, danger, and the extended family. Annu Rev Immunol, 1994, 12, 991–1045.
[155] Sinha, AA; Lopez, MT; McDevitt, HO. Autoimmune diseases: the failure of self tolerance. Science, 1990, 248, 1380–8.
[156] Goodnow, CC; Brink, R; Adams, E. Breakdown of self-tolerance in anergic B lymphocytes. Nature, 1991, 352, 532–6.
[157] Louis, JA; Chiller, JM; Weigle, WO. The ability of bacterial lipopolysaccharide tomodulate the induction of unresponsiveness to a state of immunity. Cellular parameters. J Exp Med, 1973, 138, 1481–95.
[158] Limmer, A; Sacher, T; Alferink, J; et al. Failure to induce organ-specific autoimmunity by breaking of tolerance: importance of the microenvironment. Eur J Immunol, 1998, 28, 2395–406.
[159] Gautam, AM; Lock, CB; Smilek, DE; Pearson, CI; Steinman, L; McDevitt, HO. Minimum structural requirements for peptide presentation by major histocompatibility complexclass II molecules: implications in induction of autoimmunity. Proc. Natl. Acad. Sci. U.S.A, 1994, 91, 767–71.
[160] Wucherpfennig, KW; Strominger, JL. Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein. Cell, 1995, 80, 695–705.
[161] Prinz, JC. Which T cells cause psoriasis? Clin Exp Dermatol, 1999, 24, 291–5.
[162] Chuang, TY; Stitle, L; Brashear, R; Lewis, C. Hepatitis C virus and lichen planus: Acase-control study of 340 patients. J Am Acad Dermatol, 1999, 41, 787–9.
[163] Lefort, A; Dachary, D; Vergier, B; Boiron, G. Lichen planus and vaccination against hepatitis B. Ann Dermatol Venereol, 1995, 122(10), 701-3.
[164] Tessari, G; Barba, A; Schena, D. Lichen ruber planus following the administration ofhuman anti-hepatitis B virus immunoglobulins [letter]. Acta Derm. Venereol, 1996, 76, 154.
[165] Berg, PA; Klein, R; Rocken, M. Cytokines in primary biliary cirrhosis. Semin Liver Dis, 1997, 17, 115–23.
[166] Gerlach, JT; Diepolder, HM; Jung, MC; et al. Recurrence of hepatitis C virus after loss of virus-specific CD4(+) T-cell response in acute hepatitis C. Gastroenterology, 1999, 117, 933–41.
[167] Moradpour, D; Blum, HE. Current and evolving therapies for hepatitis C. Eur. J Gastroenterol Hepatol, 1999, 11, 1199–202.
[168] Rocken, M; Urban, J; Shevach, EM. Antigen-specific activation, tolerization, and reactivation of the interleukin 4 pathway in vivo. J Exp Med, 1994, 179, 1885–93.
[169] Nemazee, D; Buerki, K. Clonal deletion of autoreactive B lymphocytes in bone marrow chimeras. Proc Natl Acad Sci USA, 1989, 86, 8039–43.
[170] Menard, L; Saadoun, D; Isnardi, I; et al. The PTPN22 allele encoding an R620W variant interferes with the removal of developing autoreactive B cells in humans. J Clin Invest, 2011, 121, 3635–44.
[171] Smilek, DE; Ehlers, MR; Nepom, GT. Restoring the balance: immunotherapeutic combinations for autoimmune disease. Dis Model Mech, 2014, 7(5), 503-13.
[172] Hartley, SB; Crosbie, J; Brink, R; Kantor, AB; Basten, A; Goodnow, CC. Elimination fromperipheral lymphoid tissues of self reactive B lymphocytes recognizing membrane bound antigens. Nature, 1991, 353, 765–9.
[173] Quách, TD; Manjarrez-Orduño, N; Adlowitz, DG; et al. Anergic responses characterize a large fraction of human autoreactive naive B cells expressing low levels of surface IgM. J Immunol, 2011, 186, 4640–8.
[174] Gauld, SB; Benschop, RJ; Merrell, KT; Cambier, JC. Maintenance of B cell anergy requires constant antigen receptor occupancy and signaling. Nat Immunol, 2005, 6, 1160–7.
[175] Cambier, JC. Autoimmunity risk alleles: hotspots in B cell regulatory signaling pathways. J Clin Invest, 2013, 123, 1928–31.
[176] Oropallo, MA; Kiefer, K; Marshak-Rothstein, A; Cancro, MP. Beyond transitional selection: New roles for BLyS in peripheral tolerance. Drug Dev Res, 2011, 72, 779–87.
[177] Treml, LS; Carlesso, G; Hoek, KL; et al. TLR stimulation modifies BLyS receptor expression in follicular and marginal zone B cells. J Immunol, 2007, 178, 7531–9.
[178] Rawlings, DJ; Schwartz, MA; Jackson, SW; Meyer-Bahlburg, A. Integration of B cell responses through Toll-like receptors and antigen receptors. Nat Rev Immunol, 2012, 12, 282–94.
[179] Amagai, M. The molecular logic of pemphigus and impetigo: the desmoglein story. Vet Dermatol, 2009, 20(5–6), 308–12.
[180] Rock, B; Martins, CR; Theofilopoulos, AN; et al. The pathogenic effect of IgG4 autoantibodies in endemicpemphigus foliaceus (fogo selvagem). N Engl J Med, 1989, 320, 1463–9.
[181] Hertl, M; Eming, R; Veldman, C. T cell control inautoimmune bullous skin disorders. J Clin Invest, 2006, 116(5), 1159–66.
[182] Liu, Z; Shapiro, SD; Zhou, X; et al. A critical role for neutrophil elastase in experimental bullous pemphigoid. J Clin Invest, 2000, 105, 113–23.
[183] Liu, Z; Shipley, JM; Vu, TH; et al. GelatinaseB-deficient mice are resistant to experimental bullous pemphigoid. J Exp Med, 1998, 188, 475–82.
[184] Liu, Z; Giudice, GJ; Swartz, SJ; et al. The role of complement in experimental bullous pemphigoid. J Clin Invest, 1995, 95, 1539–44.
[185] Stenger, S; Modlin, RL. T cell mediated immunity to Mycobacterium tuberculosis. Curr Opin Microbiol, 1999, 2, 89–93.
[186] Zinkernagel, RM. Immunology taught by viruses. Science, 1996, 271, 173–8.
[187] Krueger, GG; Langley, RG; Leonardi, C; et al. A human interleukin-12/23 monoclonalantibody for the treatment of psoriasis. N Engl J Med, 2007, 356, 580–92.
[188] Biedermann, T; Kneilling, M; Mailhammer, R; et al. Mast Cells Control Neutrophil Recruitment during TCell-mediated Delayed-type Hypersensitivity Reactions through Tumor Necrosis Factor and Macrophage Inflammatory Protein 2. J Exp Med, 2000, 192, 1441–52.
[189] Kneilling, M; Mailhammer, R; Hultner, L; et al. Direct cross talk between mast cell-TNF and TNFR1-expressing endothelia mediates local tissue inflammation. Blood, 2009, 114, 1696–706.
[190] Chen, R; Diaz L; Giudice G; Liu Z. The role of C5a in mast cell activation during sub epidermal blistering in experimetnal bullous pemphigoid. J Invest Dermatol, 2000, 114, 762.
[191] Green, EA; Flavell, RA. The temporal importance of TNFalpha expression in the development of diabetes. Immunity, 2000, 12, 459–69.
[192] Bendelac, A; Carnaud, C; Boitard, C; Bach, JF. Syngeneic transfer of autoimmunediabetes from diabetic NOD mice to healthy neonates. Requirement for both L3T4+ and Lyt-2+T cells. J Exp Med, 1987, 166, 823–32.
[193] Martin, R; McFarland, HF; McFarlin, DE. Immunological aspects of demyelinatingdiseases. Annu Rev Immunol, 1992, 10, 153–87.
[194] Salou, M; Nicol, B; Garcia, A; Laplaud, DA. Involvement of CD8(+) T Cells in Multiple Sclerosis. Front Immunol, 2015, 6, 604.
[195] Austin, LM; Ozawa, M; Kikuchi, T; Walters, IB; Krueger, JG. The majority of epidermalT cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-γ, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J Invest Dermatol, 1999, 113, 752–9.
[196] Vollmer, S; Menssen, A; Trommler, P; Schendel, D; Prinz, JC. T lymphocytes derived from skin lesions of patients with psoriasis vulgaris express a novel cytokine pattern that is distinct from that of T helper type 1 and T helper type 2 cells. Eur J Immunol, 1994, 24, 2377–82.
[197] Feldmann, M; Brennan, FM; Maini, RN. Role of cytokines in rheumatoid arthritis. Annu Rev Immunol, 1996, 14, 397–440.
[198] Mease, PJ; Goffe, BS; Metz, J; VanderStoep, A; Finck, B; Burge, DJ. Etanercept inthe treatment of psoriatic arthritis and psoriasis: a randomised trial. Lancet, 2000, 356, 385–90.
[199] Tirado-Sánchez, A; Ponce-Olivera, RM; Vazquez-González, D; Bonifaz, A. Th-17 and the lack of efficacy of ustekinumab in pemphigus vulgaris. Dermatol Online J, 2013 15, 19(3), 15.
[200] Abrams, JR; Kelley, SL; Hayes, E; et al. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells. J Exp Med, 2000, 192, 681–94.
[201] Krueger, GG; Ellis, CN. Alefacept therapy produces remission for patients with chronicplaque psoriasis. Br J Dermatol, 2003, 148, 784–8.
[202] Biedermann, T; Mailhammer, R; Mai, A; et al. Reversal of established delayed type hypersensitivity reactionsfollowing therapy with IL-4 or antigen-specific Th2 cells. Eur J Immunol, 2001, 31, 1582–91.
[203] Amagai, M. Adhesion molecules. I: keratinocytekeratinocyteinteractions; cadherins and pemphigus. J Invest Dermatol, 1995, 104(1), 146–52.
[204] Gniadecki, R. Desmoglein autoimmunity in the pathogenesis of pemphigus. Autoimmunity, 2006, 39(7), 541-7.
[205] Patel, SD; Chen, CP; Bahna, F; Honig, B; Shapiro, L. Cadherin-mediated cell-cell adhesion, sticking togetheras a family. Curr Opin Struct Biol, 2003, 13(6), 690–8.
[206] Blaschuk, OW; Sullivan, R; David, S; Pouliot, Y. Identification of a cadherin cell adhesion recognitionsequence. Dev Biol, 1990, 139(1), 227–9.
[207] Runswick, SK; O’Hare, MJ; Jones, L; Streuli, CH; Garrod, DR. Desmosomal adhesion regulates epithelialmorphogenesis and cell positioning. Nat Cell Biol, 2001, 3(9), 823–30.
[208] Tselepis, C; Chidgey, M; North, A; Garrod, D. Desmosomal adhesion inhibits invasive behavior. Proc Natl Acad Sci U S A, 1998, 95(14), 8064–9.
[209] Garrod, D; Chidgey, M; North, A. Desmosomes: differentiation, development, dynamics and disease. Curr Opin Cell Biol, 1996, 8(5), 670–8.
[210] Hirano, S; Nose, A; Hatta, K; Kawakami, A; Takeichi, M. Calcium-dependent cell-cell adhesion molecules (cadherins), subclass specificities and possible involvement of actin bundles. J Cell Biol, 1987, 105(6 Pt 1), 2501–10.
[211] Yap, AS; Brieher, WM; Gumbiner, BM. Molecular andfunctional analysis of cadherin-based adherens junctions. Annu Rev Cell Dev Biol, 1997, 13, 119–46.
[212] Green, KJ; Gaudry, CA. Are desmosomes more thantethers for intermediate filaments? Nat Rev Mol Cell Biol, 2000, 1(3), 208–16.
[213] Bornslaeger, EA; Corcoran, CM; Stappenbeck, TS; Green, KJ. Breaking the connection: displacement ofthe desmosomal plaque protein desmoplakin fromcell-cell interfaces disrupts anchorage of intermediatefilament bundles and alters intercellular junctionassembly. J Cell Biol, 1996, 134(4), 985–1001.
[214] Hirai, Y; Nose, A; Kobayashi, S; Takeichi, M. Expression and role of E- and P-cadherin adhesion molecules inembryonic histogenesis. II. Skin morphogenesis. Development, 1989, 105(2), 271–7.
[215] Delva, E; Tucker, DK; Kowalczyk, AP. The desmosome. Cold Spring Harb Perspect Biol, 2009, 1(2), a002543.
[216] Franke, WW. Discovering the molecular componentsof intercellular junctions—a historical view. Cold Spring Harb Perspect Biol, 2009, 1(3), a003061.
[217] Skerrow, CJ; Matoltsy, AG. Isolation of epidermal desmosomes. J Cell Biol, 1974, 63(2 Pt 1), 515–23.
[218] Koch, PJ; Walsh, MJ; Schmelz, M; Goldschmidt, MD; Zimbelmann, R; Franke, WW. Identification of desmoglein, a constitutive desmosomal glycoprotein, as amember of the cadherin family of cell adhesionmolecules. Eur J Cell Biol, 1990, 53(1), 1–12.
[219] Dusek, RL; Godsel, LM; Green, KJ. Discriminating roles of desmosomal cadherins: beyond desmosomal adhesion. J Dermatol Sci, 2007, 45(1), 7–21.
[220] Cowley, CM; Simrak, D; Marsden, MD; King, IA; Arnemann, J; Buxton, RS. A YAC contig joiningthe desmocollin and desmoglein loci on human. Chromo some 18 and ordering of the desmocollingenes. Genomics, 1997, 42(2), 208–16.
[221] Al-Amoudi, A; Diez, DC; Betts, MJ; Frangakis, AS. Themolecular architecture of cadherins in native epidermaldesmosomes. Nature, 2007, 450(7171), 832–7.
[222] Boggon, TJ; Murray, J; Chappuis-Flament, S; Wong, E; Gumbiner, BM; Shapiro, L. C-cadherin ectodomain structure and implications for cell adhesion mechanisms. Science, 2002, 296(5571), 1308–13.
[223] Amagai, M; Karpati, S; Klaus-Kovtun, V; Udey, MC; Stanley, JR. Extracellular domain of pemphigus vulgarisantigen (desmoglein 3) mediates weak hemophilic adhesion. J Invest Dermatol, 1994, 102(4), 402–8.
[224] Syed, SE; Trinnaman, B; Martin, S; Major, S; Hutchinson, J; Magee, AI. Molecular interactionsbetween desmosomal cadherins. Biochem J, 2002, 362(Pt 2), 317–27.
[225] Waschke, J; Bruggeman, P; Baumgartner, W; Zillikens, D; Drenckhahn, D. Pemphigus foliaceus IgG causes dissociationof desmoglein 1-containing junctions without blocking desmoglein 1 transinteraction. J Clin Invest, 2005, 115(11), 3157–65.
[226] Nie, Z; Merritt, A; Rouhi-Parkouhi, M; Tabernero, L; Garrod, D. Membrane-impermeable cross-linkingprovides evidence for hemophilic, isoform-specific binding of desmosomal cadherins in epithelial cells. J Biol Chem, 2011, 286(3), 2143–54.
[227] Spindler, V; Heupel, WM; Efthymiadis, A; et al. Desmocollin 3-mediated binding is crucial for keratinocyte cohesion and is impaired in pemphigus. J Biol Chem, 2009, 284(44), 30556–64.
[228] Chitaev, NA; Troyanovsky, SM. Direct Ca2+-dependent heterophilic interaction between desmosomalcadherins, desmoglein and desmocollin, contributes to cell-cell adhesion. J Cell Biol, 1997, 138(1), 193–201.
[229] Pokutta, S; Weis, WI. Structure and mechanism of cadherins and catenins in cellecell contacts. Annu Rev Cell Dev Biol, 2007, 23, 237e61.
[230] Aberle, H; Bierkamp, C; Torchard, D; et al. The humanplakoglobin gene localizes on chromosome 17q21 and is subjected to loss of heterozygosity in breast and ovarian cancers. Proc Natl Acad Sci U S A, 1995, 92(14), 6384–8.
[231] Palka, HL; Green, KJ. Roles of plakoglobin end domains in desmosome assembly. J Cell Sci, 1997, 110(Pt 19), 2359–71.
[232] Peifer, M; McCrea, PD; Green, KJ; Wieschaus, E; Gumbiner, BM. The vertebrate adhesive junction proteins beta-catenin and plakoglobin and the Drosophilasegment polarity gene armadillo form a multi gene family with similar properties. J Cell Biol, 1992, 118(3), 681–91.
[233] Choi, HJ; Gross, JC; Pokutta, S; Weis, WI. Interactions of plakoglobin and beta-catenin with desmosomal cadherins: basis of selective exclusion of alpha- andbeta-catenin from desmosomes. J Biol Chem, 2009, 284(46), 31776–88.
[234] Kowalczyk, AP; Bornslaeger, EA; Borgwardt, JE; et al. The amino-terminal domain of desmoplakin binds to plakoglobin and clusters desmosomal cadherin plakoglobin complexes. J Cell Biol, 1997, 139(3), 773–84.
[235] Troyanovsky, SM; Troyanovsky, RB; Eshkind, LG; Krutovskikh, VA; Leube, RE; Franke, WW. Identification of the plakoglobin-binding domain indesmoglein and its role in plaque assembly and intermediatefilament anchorage. J Cell Biol, 1994, 127(1), 151–60.
[236] Troyanovsky, SM; Troyanovsky, RB; Eshkind, LG; Leube, RE, Franke, WW. Identification of amino acid sequence motifs in desmocollin, a desmosomal glycoprotein, that are required for plakoglobin binding and plaque formation. Proc Natl Acad Sci U S A, 1994, 91(23), 10790–4.
[237] Bonne, S; van Hengel, J; van Roy, F. Chromosomal mapping of human armadillo genes belonging to thep120(ctn)/plakophilin subfamily. Genomics, 1998, 51(3), 452–4.
[238] Schmidt, A; Langbein, L; Pratzel, S; Rode, M; Rackwitz, HR; Franke, WW. Plakophilin 3—a novel cell-type specific desmosomal plaque protein. Differentiation, 1999, 64(5), 291–306.
[239] Mertens, C; Kuhn, C; Franke, WW. Plakophilins 2a and 2b: constitutive proteins of dual location in the karyoplasms and the desmosomal plaque. J Cell Biol, 1996, 135(4), 1009–25.
[240] Hatzfeld, M; Nachtsheim, C. Cloning andcharacterization of a new armadillo family member, p0071, associated with the junctional plaque: evidence for a subfamily of closely related proteins. J Cell Sci, 1996, 109(Pt 11), 2767–78.
[241] Jefferson, JJ; Ciatto, C; Shapiro, L; Liem, RK. Structuralanalysis of the plakin domain of bullous pemphigoidantigen1 (BPAG1) suggests that plakins are members of the spectrin superfamily. J Mol Biol, 2007, 366(1), 244–57.
[242] Armstrong, DK; McKenna, KE; Purkis, PE; et al. Haploinsufficiency of desmoplakin causes a striate subtype of palmoplantar keratoderma. Hum Mol Genet, 1999, 8(1), 143–8.
[243] Hatsell, S; Cowin, P. Deconstructing desmoplakin. Nat Cell Biol, 2001, 3(12), E270–2.
[244] Green, KJ; Parry, DA; Steinert, PM; et al. Structure ofthe human desmoplakins. Implications for function in the desmosomal plaque. J Biol Chem, 1990, 265(5), 2603–12.
[245] Andra, K; Lassmann, H; Bittner, R; et al. Targetedinactivation of plectin reveals essential function in maintaining the integrity of skin, muscle, and heart cytoarchitecture. Genes Dev, 1997, 11(23), 3143–56.
[246] Pulkkinen, L; Smith, FJ; Shimizu, H; et al. Homozygous deletion mutations in the plectin gene (PLEC1) inpatients with epidermolysis bullosa simplex associated with late-onset muscular dystrophy. Hum Mol Genet, 1996, 5(10), 1539–46.
[247] Vasioukhin, V; Bowers, E; Bauer, C; Degenstein, L; Fuchs, E. Desmoplakin is essential in epidermal sheet formation. Nat Cell Biol, 2001, 3(12), 1076–85.
[248] Hu, P; O’Keefe, EJ; Rubenstein, DS. Tyrosine phosphorylation of human keratinocyte b-catenin and plakoglobin reversibly regulates their binding to E-cadherin and a-catenin. J Invest Dermatol, 2001, 117, 1059e67.
[249] Yin, T; Getsios, S; Caldelari, R; Godsel, LM; Kowalczyk, AP; Muller, EJ; et al. Mechanisms of plakoglobin-dependent adhesion: desmosome-specific functions in assembly and regulation by epidermal growth factor receptor. J Biol Chem, 2005, 280, 40355e63.
[250] Joly, P; Litrowski, N. Pemphigus group (vulgaris, vegetans, foliaceus, herpetiformis, brasiliensis). Clin Dermatol, 2011, 29(4), 432–6.
[251] Diaz, LA; Giudice, GJ. End of the century overview ofskin blisters. Arch Dermatol, 2000, 136(1), 106–12.
[252] Ding, X; Aoki, V; Mascaro, Jr. JM; Lopez-Swiderski, A; Diaz, LA; Fairley, JA. Mucosal and mucocutaneous (generalized) pemphigus vulgaris show distinct autoantibody profiles. J Invest Dermatol, 1997, 109(4), 592–6.
[253] Amagai, M; Karpati, S; Prussick, R; Klaus-Kovtun, V; Stanley, JR. Autoantibodies against the aminoterminal cadherin-like binding domain of pemphigus vulgaris antigen are pathogenic. J Clin Invest, 1992, 90(3), 919–26.
[254] Ding, X; Diaz, LA; Fairley, JA; Giudice, GJ; Liu, Z. The anti-desmoglein 1 autoantibodies in pemphigus vulgaris sera are pathogenic. J Invest Dermatol, 1999, 112(5), 739–43.
[255] Amagai, M; Hashimoto, T; Shimizu, N; Nishikawa, T. Absorption of pathogenic autoantibodies by the extracellular domain of pemphigus vulgaris antigen (Dsg3) producedby baculovirus. J Clin Invest, 1994, 94(1), 59–67.
[256] Amagai, M; Klaus-Kovtun, V; Stanley, JR. Autoantibodies against a novel epithelial cadherin in pemphigus vulgaris, a disease of cell adhesion. Cell, 1991, 67(5), 869–77.
[257] Tsunoda, K; Ota, T; Saito, M; Hata, T; Shimizu, A; Ishiko, A; et al. Pathogenic relevance of IgG and IgM antibodies against desmoglein 3 in blister formation in pemphigus vulgaris. Am J Pathol, 2011, 179(2), 795–806.
[258] Amagai, M; Komai, A; Hashimoto, T; Shirakata, Y; Hashimoto, K; Yamada, T; et al. Usefulness of enzyme-linked immunosorbent assay using recombinant desmogleins 1 and 3 for serodiagnosis of pemphigus. Br J Dermatol, 1999, 140(2), 351–7.
[259] Mahoney, MG; Wang, ZH; Stanley, JR. Pemphigusvulgaris and pemphigus foliaceus antibodies arepathogenic in plasminogen activator knockout mice. JInvest Dermatol, 1999, 113(1), 22–5.
[260] Ota, T; Aoki-Ota, M; Tsunoda, K; Simoda, K; Nishikawa, T; Amagai, M; et al. Auto-reactive B cells againstperipheral antigen, desmoglein 3, escape from tolerancemechanism. Int Immunol, 2004, 16(10), 1487–95.
[261] Mouquet, H; Musette, P; Gougeon, ML; Jacquot, S; Lemercier, B; Lim, A; et al. B-cell depletion immunotherapy in pemphigus: effects on cellular and humoral immune responses. J Invest Dermatol, 2008, 128(12), 2859–69.
[262] Eming, R; Nagel, A; Wolff-Franke, S; Podstawa, E; Debus, D; Hertl, M. Rituximab exerts a dual effect in pemphigus vulgaris. J Invest Dermatol, 2008, 128(12), 2850–8.
[263] Colliou, N; Picard, D; Caillot, F; Calbo, S; Le Corre, S; Lim, A; et al. Long-term remissions of severe pemphigus after rituximab therapy are associated with prolonged failure of desmoglein B cell response. Sci Transl Med, 2013, 5(175), 175ra30.
[264] Wucherpfennig, KW; Yu, B; Bhol, K; Monos, DS; Argyris, E; Karr, RW; et al. Structural basis for major histocompatibility complex (MHC)-linked susceptibility to autoimmunity: charged residues of a single MHC binding pocket confer selective presentationof self-peptides in pemphigus vulgaris. Proc Natl Acad Sci U S A, 1995, 92(25), 11935–9.
[265] Lin, MS; Swartz, SJ; Lopez, A; Ding, X; Fernandez-Vina, MA; Stastny, P; et al. Development and characterization of desmoglein-3 specific T cells from patients with pemphigus vulgaris. J Clin Invest, 1997, 99(1), 31–40.
[266] Veldman, C; Stauber, A; Wassmuth, R; Uter, W; Schuler, G; Hertl, M. Dichotomy of autoreactive Th1 and Th2 cell responses to desmoglein 3 in patients with pemphigus vulgaris (PV) and healthy carriers of PV-associated HLA class II alleles. J Immunol, 2003, 170(1), 635–42.
[267] Riechers, R; Grotzinger, J; Hertl, M. HLA class II restriction of autoreactive T cell responses in pemphigus vulgaris: review of the literature and potential applications for the development of a specific immunotherapy. Autoimmunity, 1999, 30(3), 183–96.
[268] Veldman, CM; Gebhard, KL; Uter, W; et al. T cell recognition of desmoglein 3 peptides in patients with pemphigus vulgaris and healthy individuals. J Immunol, 2004, 172(6), 3883–92.
[269] Tony, HP; Burmester, G; Schulze-Koops, H; Grunke, M; Henes, J; Kotter, I; et al. Safety and clinical outcomesof rituximab therapy in patients with different autoimmune diseases: experience from a national registry(GRAID). Arthritis Res Ther, 2011, 13(3), R75.
[270] Ahmed, AR; Spigelman, Z; Cavacini, LA; Posner, MR. Treatment of pemphigus vulgaris with rituximab and intravenous immune globulin. N Engl J Med, 2006, 355(17), 1772–9.
[271] Joly, P; et al. A single cycle of rituximab for the treatment of severe pemphigus. N Engl J Med, 2007, 357(6), 545–52.
[272] Schmidt, E; Goebeler, M; Zillikens, D. Rituximab in severe pemphigus. Ann N Y Acad Sci, 2009, 1173, 683–91.
[273] Nagel, A; Hertl, M; Eming, R. B-cell-directed therapy for inflammatory skin diseases. J Invest Dermatol, 2009, 129(2), 289–301.
[274] Nagel, A; Podstawa, E; Eickmann, M; Muller, HH; Hertl, M; Eming, R. Rituximab mediates a strong elevation of B-cell-activating factor associated with increased pathogen-specific IgG but not autoantibodies in pemphigus vulgaris. J Invest Dermatol, 2009, 129(9), 2202–10.
[275] Hoss, DM; Shea, CR; Grant-Kels, JM. Neutrophilic spongiosis in pemphigus. Arch Dermatol, 1996, 132(3), 315–8.
[276] Sekiguchi, M; Futei, Y; Fujii, Y; Iwasaki, T; Nishikawa, T; Amagai, M. Dominant autoimmune epitopes recognized by pemphigus antibodies map to the N-terminal adhesive region of desmogleins. J Immunol, 2001, 167(9), 5439–48.
[277] Stanley, JR; Amagai, M. Pemphigus, bullous impetigo, and the staphylococcal scalded-skin syndrome. N Engl J Med, 2006, 355(17), 1800–10.
[278] James, KA; Culton, DA; Diaz, LA. Diagnosis and clinical features of pemphigus foliaceus. Dermatol Clin, 2011, 29(3), 405–12; viii.
[279] Lin, MS; Fu, CL; Aoki, V; Hans-Filho, G; Rivitti, EA; Moraes, JR; et al. Desmoglein-1-specific T lymphocytes from patients with endemic pemphigus foliaceus (fogo selvagem). J Clin Invest, 2000, 105(2), 207–13.
[280] Gebhard, KL; Veldman, CM; Wassmuth, R; Schultz, E; Schuler, G; Hertl, M. Ex vivo analysis of desmoglein1-responsive T-helper (Th) 1 and Th2 cells in patients with pemphigus foliaceus and healthy individuals. Exp Dermatol, 2005, 14(8), 586–92.
[281] Warren, SJ; Lin, MS; Giudice, GJ; et al. The prevalence of antibodies against desmoglein 1 in endemic pemphigus foliaceus in Brazil. Cooperative Group on Fogo Selvagem Research. N Engl J Med, 2000, 343(1), 23–30.
[282] Qaqish, BF; Prisayanh, P; Qian, Y; et al. Development of an IgG4-based predictorof endemic pemphigus foliaceus (fogo selvagem). J Invest Dermatol, 2009, 129(1), 110–8.
[283] Hacker-Foegen, MK; Janson, M; Amagai, M; Fairley, JA; Lin, MS. Pathogenicity and epitope characteristicsof anti-desmoglein-1 from pemphigus foliaceus patients expressing only IgG1 autoantibodies. J Invest Dermatol, 2003, 121(6), 1373–8.
[284] Qian, Y; Jeong, JS; Maldonado, M; et al. Cutting edge: Brazilianpemphigus foliaceus anti-desmoglein 1 autoantibodiescross-react with sand fly salivary LJM11 antigen. J Immunol, 2012, 189(4), 1535–9.
[285] Culton, DA; Qian, Y; Li, N; et al. Advances in pemphigus and its endemic pemphigus foliaceus (Fogo Selvagem) phenotype: a paradigm of human autoimmunity. J Autoimmun, 2008, 31(4), 311–24.
[286] Mimouni, D; Anhalt, GJ; Lazarova, Z; et al. Paraneoplastic pemphigusin children and adolescents. Br J Dermatol, 2002, 147(4), 725–32.
[287] Anhalt, GJ. Paraneoplastic pemphigus. J Investig Dermatol Symp Proc, 2004, 9(1), 29–33.
[288] Billet, S; Grando, S; Pittelkow, M. Paraneoplastic autoimmune multiorgan syndrome: review of the literature and support for a cytotoxic role in pathogenesis. Autoimmunity, 2006, 39(7), 617–30.
[289] Schepens, I; Jaunin, F; Begre, N; et al. The protease inhibitor alpha-2-macroglobulin-like-1 is the p170 antigen recognized by paraneoplastic pemphigus autoantibodiesin human. PLoS One, 2010, 5(8), e12250.
[290] Anhalt, GJ; Kim, SC; Stanley, JR; et al. Paraneoplasticpemphigus. An autoimmune mucocutaneous disease associated with neoplasia. N Engl J Med, 1990, 323(25), 1729–35.
[291] Amagai, M; Nishikawa, T; Nousari, HC; Anhalt, GJ; Hashimoto, T. Antibodies against desmoglein 3 (pemphigus vulgaris antigen) are present in sera from patients with paraneoplastic pemphigus and causeacantholysis in vivo in neonatal mice. J Clin Invest, 1998, 102(4), 775–82.
[292] Cozzani, E; Di Zenzo, G; Calabresi, V; et al. Antidesmoplakin antibodies in erythema multiforme and Stevens-Johnson syndrome sera: pathogenic or epiphenomenon? Eur J Dermatol, 2011, 21(1), 32–6.
[293] Fukiwake, N; Moroi, Y; Urabe, K; Ishii, N; Hashimoto, T; Furue, M. Detection of autoantibodies to desmoplakin in a patient with oral erythema multiforme. Eur J Dermatol, 2007, 17(3), 238–41.
[294] Hashimoto, T; Komai, A; Futei, Y; Nishikawa, T; Amagai, M. Detection of IgA autoantibodies to desmogleins by an enzyme-linked immunosorbent assay: the presence of new minor subtypes of IgA pemphigus. Arch Dermatol, 2001, 137(6), 735–8.
[295] Nishikawa, T; Hashimoto, T; Teraki, Y; Ebihara, T. Theclinical and histopathological spectrum of IgA pemphigus. Clin Exp Dermatol, 1991, 16(5), 401–2.
[296] Hashimoto, T. Immunopathology of IgA pemphigus. Clin Dermatol, 2001, 19(6), 683–9.
[297] Hashimoto, T; Kiyokawa, C; Mori, O; Miyasato, M; Chidgey, MA; Garrod, DR; et al. Human desmocollin1 (Dsc1) is an autoantigen for the subcorneal pustular dermatosis type of IgA pemphigus. J Invest Dermatol, 1997, 109(2), 127–31.
[298] Duker, I; Schaller, J; Rose, C; Zillikens, D; Hashimoto, T; Kunze, J. Subcorneal pustular dermatosis-type IgA pemphigus with autoantibodies to desmocollins 1, 2, and 3. Arch Dermatol, 2009, 145(10), 1159–62.
[299] Ebihara, T; Hashimoto, T; Iwatsuki, K; et al. Autoantigens for IgA antiintercellular antibodies of intercellular IgA vesiculopustulardermatosis. J Invest Dermatol, 1991, 97(4), 742–5.
[300] Karpati, S; Amagai, M; Liu, WL; Dmochowski, M; Hashimoto, T; Horvath, A. Identification of desmoglein1 as autoantigen in a patient with intraepidermalneutrophilic IgA dermatosis type of IgApemphigus. Exp Dermatol, 2000, 9(3), 224–8.
[301] Tajima, M; Mitsuhashi, Y; Irisawa, R; Amagai, M; Hashimoto, T; Tsuboi, R. IgA pemphigus reacting exclusivelyto desmoglein 3. Eur J Dermatol, 2010, 20(5), 626–9.
[302] Geller, S; Gat, A; Zeeli, T; et al. The expanding spectrum of IgA pemphigus: a case report and review of the literature. Br J Dermatol, 2014, 171(3), 650–6.
[303] Tsuruta, D; Ishii, N; Hamada, T; et al. IgA pemphigus. Clin Dermatol, 2011, 29(4), 437–42.
[304] Kubo, A; Amagai, M; Hashimoto, T; et al. Herpeti form pemphigus showing reactivity with pemphigus vulgaris antigen (desmoglein 3). Br J Dermatol, 1997, 137(1), 109–13.
[305] Kasperkiewicz, M; Kowalewski, C; Jablonska, S. Pemphigus herpetiformis: from first description until now. J Am Acad Dermatol, 2014, 70(4), 780–7.
[306] Ishii, K; Amagai, M; Komai, A; et al. Desmoglein 1 and desmoglein 3 are the target autoantigens in herpetiform pemphigus. Arch Dermatol, 1999, 135(8), 943–7.
[307] On, HR; Hashimoto, T; Kim, SC. Pemphigus herpetiformis with IgG autoantibodies to desmoglein 1 and desmocollin1. Br J Dermatol, 2015, 172(4), 1144-6.
[308] Rafei, D; Muller, R; Ishii, N; et al. IgG autoantibodies against desmocollin3 in pemphigus sera induces loss of keratinocyteadhesion. Am J Pathol, 2011, 178(2), 718–23.
[309] Nakamura, Y; Takahata, H; Teye, K; Ishii, N; Hashimoto, T; Muto, M. A case of pemphigus herpetiformis-like atypical pemphigus with IgG anti-desmocollin 3 antibodies. Br J Dermatol, 2014, 171(6), 1588-90.
[310] Ohyama, B; Nishifuji, K; Chan, PT; et al. Epitope spreading is rarelyfound in pemphigus vulgaris by large-scale longitudinalstudy using desmoglein 2-based swapped molecules. J Invest Dermatol, 2012, 132(4), 1158–68.
[311] Loiseau, P; Lecleach, L; Prost, C; et al. HLA class II polymorphism contributes to specify desmogleinderived peptides in pemphigus vulgaris and pemphigusfoliaceus. J Autoimmun, 2000, 15(1), 67–73.
[312] Li, N; Aoki, V; Hans-Filho, G; Rivitti, EA; Diaz, LA. Therole of intramolecular epitope spreading in the pathogenesisof endemic pemphigus foliaceus (fogo selvagem). J Exp Med, 2003, 197(11), 1501–10.
[313] Futei, Y; Amagai, M; Sekiguchi, M; Nishifuji, K; Fujii, Y; Nishikawa, T. Use of domain-swapped molecules forconformational epitope mapping of desmoglein 3 in pemphigus vulgaris. J Invest Dermatol, 2000, 115(5), 829–34.
[314] Shapiro, L; Fannon, AM; Kwong, PD; et al. Structural basis of cell-cell adhesion by cadherins. Nature, 1995, 374(6520), 327–37.
[315] Anhalt, GJ; Patel, HP; Labib, RS; Diaz, LA; Proud, D. Dexamethasone inhibits plasminogen activator activityin experimental pemphigus in vivo but does notblock acantholysis. J Immunol, 1986, 136(1), 113–7.
[316] Anhalt, GJ; Till, GO; Diaz, LA; Labib, RS; Patel, HP; Eaglstein, NF. Defining the role of complement inexperimental pemphigus vulgaris in mice. J Immunol, 1986, 137(9), 2835–40.
[317] Rock, B; Labib, RS; Diaz, LA. Monovalent Fab’ immunoglobulin fragments from endemic pemphigus foliaceus autoantibodies reproduce the human disease inneonatal Balb/c mice. J Clin Invest, 1990, 85(1), 296–9.
[318] Tsunoda, K; Ota, T; Aoki, M; et al. Induction of pemphigus phenotypeby a mouse monoclonal antibody against the aminoterminaladhesive interface of desmoglein 3. J Immunol, 2003, 170(4), 2170–8.
[319] Heupel, WM; Zillikens, D; Drenckhahn, D; Waschke J. Pemphigus vulgaris IgG directly inhibit desmoglein3-mediated transinteraction. J Immunol, 2008, 181(3), 1825–34.
[320] Waschke, J; Menendez-Castro, C; Bruggeman, P; et al. Imaging and force spectroscopy on desmoglein 1using atomic force microscopy reveal multivalent Ca(2+)-dependent, low-affinity trans-interaction. J Membr Biol, 2007, 216(2–3), 83–92.
[321] Waschke, J. The desmosome and pemphigus. Histochem Cell Biol, 2008, 130(1), 21–54.
[322] Seishima, M; Esaki, C; Osada, K; Mori, S; Hashimoto, T; Kitajima, Y. Pemphigus IgG, but not bullous pemphigoid IgG, causes a transient increase in intracellularcalcium and inositol 1, 4, 5-triphosphate in DJM-1cells, a squamous cell carcinoma line. J Invest Dermatol, 1995, 104(1), 33–7.
[323] Aoyama, Y; Kitajima, Y. Pemphigus vulgaris-IgG causes a rapid depletion of desmoglein 3 (Dsg3) from the Triton X-100 soluble pools, leading to the formation of Dsg3-depleted desmosomes in a humansquamous carcinoma cell line, DJM-1 cells. J Invest Dermatol, 1999, 112(1), 67–71.
[324] Aoyama, Y; Owada, MK; Kitajima, Y. A pathogenic autoantibody, pemphigus vulgaris-IgG, induces phosphorylation of desmoglein 3, and its dissociation from plakoglobin in cultured keratinocytes. Eur J Immunol, 1999, 29(7), 2233–40.
[325] Calkins, CC; Setzer, SV; Jennings, JM; et al. Desmogleinendocytosis and desmosome disassembly are coordinated responses to pemphigus autoantibodies. J Biol Chem, 2006, 281(11), 7623–34.
[326] Kitajima, Y; Aoyama, Y; Seishima, M. Transmembranesignaling for adhesive regulation of desmosomes andhemidesmosomes, and for cell-cell detachment induced by pemphigus IgG in cultured keratinocytes: involvement of protein kinase C. J Investig Dermatol Symp Proc, 1999, 4(2), 137–44.
[327] Sato, M; Aoyama, Y; Kitajima, Y. Assembly pathway ofdesmoglein 3 to desmosomes and its perturbation by pemphigus vulgaris-IgG in cultured keratinocytes, asrevealed by time-lapsed labeling immunoelectronmicroscopy. Lab Invest, 2000, 80(10), 1583–92.
[328] Shu, E; Yamamoto, Y; Sato-Nagai, M; Aoyama, Y; Kitajima, Y. Pemphigus vulgaris-IgG reduces the desmoglein 3/desmocollin 3 ratio on the cell surface in cultured keratinocytes as revealed by doublestainingimmunoelectron microscopy. J Dermatol Sci, 2005, 40(3), 209–11.
[329] Seko, YS; Cole, W; Kasprzak, BA; et al. The role of cytokine mRNA stability in the pathogenesis of autoimmune disease. Autoimmunity Rev, 2006, 5(5), 299–305.
[330] Saklatvala, J. The p38 MAP kinase pathway as a therapeutic target in inflammatory disease. Curr Opin Pharmacol, 2004, 4(4), 372–7.
[331] Brook, MG; Sully, AR. Regulation of tumour necrosis factor a mRNA stability by the mitogenactivated protein kinase p38 signalling cascade,” FEBS Letters, 2000, 483, 57–61.
[332] Mavropoulos, AG; Sully, AP; Clark, AR. Stabilization of IFN-g mRNA by MAPK p38 in IL-12- and IL-18-stimulated human NK cells. Blood, 2005, 105, 282–8.
[333] Coulthard, LR; White, DE; Jones, DL; McDermott, MF; Burchill, SA. p38MAPK: stress responses from molecular mechanisms to therapeutics. Trends Mol Med, 2009, 15, 369–79.
[334] Mavropoulos, A; Orfanidou, T; Liaskos, C; et al. p38 mitogen-activated protein kinase (p38 MAPK)-mediated autoimmunity: lessons to learn from ANCA vasculitis and Pemphigus vulgaris. Autoimmun Rev, 2013, 12, 580–90.
[335] Johansen, C; Funding, AT; Otkjaer, K; et al. Protein expression of TNF-a in psoriatic skin is regulated at a posttranscriptional level by MAPK-activated protein kinase 2. J Immunol, 2006, 176, 1431–8.
[336] Mavropoulos, A; Smyk, D; Rigopoulou, EI; Bogdanos, DP. Human peripheral blood mononuclear cell culture for flow cytometric analysis of phosphorylated mitogen-activated protein kinases. Methods Mol Biol, 2012, 806, 275–85.
[337] Berkowitz, P; Chua, M; Liu, Z; Diaz, LA; Rubenstein, DS. Autoantibodies in the autoimmune diseasepemphigus foliaceus induce blistering via p38mitogen- activated protein kinase-dependent signalingin the skin. Am J Pathol, 2008, 173(6), 1628–36.
[338] Berkowitz, P; Diaz, LA; Hall, RP; Rubenstein, DS. Induction of p38MAPK and HSP27 phosphorylationin pemphigus patient skin. J Invest Dermatol, 2008, 128(3), 738–40.
[339] Berkowitz, P; Hu, P; Liu, Z; et al. Desmosome signaling, inhibition ofp38MAPK prevents pemphigus vulgaris IgG-induced cytoskeleton reorganization. J Biol Chem, 2005, 280(25), 23778–84.
[340] Cuenda, A; Rousseau, S. p38 MAP-kinases pathway regulation, function and role in human diseases. Biochim Biophys Acta, 2007, 1773(8), 1358–75.
[341] Schmidt, E; Gutberlet, J; Siegmund, D; Berg, D; Wajant, H; Waschke, J. Apoptosis is not required foracantholysis in pemphigus vulgaris. Am J Physiol, 2009, 296(1), C162–72.
[342] Lee, HE; Berkowitz, P; Jolly, PS; Diaz, LA; Chua, MP; Rubenstein, DS. Biphasic activation of p38MAPKsuggests that apoptosis is a downstream event inpemphigus acantholysis. J Biol Chem, 2009, 284(18), 12524–32.
[343] Nys, K; Van Laethem, A; Michiels, C; et al. Ap38(MAPK)/HIF-1 pathway initiated by UVB irradiationis required to induce Noxa and apoptosis of human keratinocytes. J Invest Dermatol, 2010, 130(9), 2269–76.
[344] Li, N; Zhao, M; Wang, J; Liu, Z; Diaz, LA. Involvementof the apoptotic mechanism in pemphigus foliaceusautoimmune injury of the skin. J Immunol, 2009, 182(1), 711–7.
[345] Gniadecki, R; Jemec, GB; Thomsen, BM; Hansen, M. Relationship between keratinocyte adhesion anddeath: anoikis in acantholytic diseases. Arch Dermatol Res, 1998, 290(10), 528–32.
[346] Rodrigues, DB; Pereira, SA; dos Reis, MA; et al. In situ detection of infl ammatory cytokines and apoptosisin pemphigus foliaceus patients. Arch Pathol Lab Med, 2009, 133(1), 97–100.
[347] Puviani, M; Marconi, A; Cozzani, E; Pincelli, C. Fasligand in pemphigus sera induces keratinocyte apoptosisthrough the activation of caspase-8. J Invest Dermatol, 2003, 120(1), 164–7.
[348] Li, J; Bu, DF; Huang, YC; Zhu, XJ. Role of autoantibodiesagainst the linker subdomains of envoplakin andperiplakin in the pathogenesis of paraneoplastic pemphigus. Chin Med J (Engl), 2009, 122(5), 486–95.
[349] Schmidt, E; Waschke, J. Apoptosis in pemphigus. Autoimmun Rev, 2009, 8(7), 533–7.
[350] Muller, E; Caldelari, R; De Bruin, A; et al. Pathogenesis in pemphigus vulgaris: a central role for the armadilloprotein plakoglobin. J Invest Dermatol, 2000, 115(2), 332.
[351] Williamson, L; Hunziker, T; Suter, MM; Muller, EJ. Nuclear c-Myc: a molecular marker for early stagepemphigus vulgaris. J Invest Dermatol, 2007, 127(6), 1549–55.
[352] Futamura, S; Martins, C; Rivitti, EA; Labib, RS; Diaz, LA; Anhalt, GJ. Ultrastructural studies of acantholysisinduced in vivo by passive transfer of IgG fromendemic pemphigus foliaceus (Fogo Selvagem). J Invest Dermatol, 1989, 93(4), 480–5.
[353] Takahashi, Y; Patel, HP; Labib, RS; Diaz, LA; Anhalt, GJ. Experimentally induced pemphigus vulgaris in neonatal BALB/c mice: a time-course study of clinical, immunologic, ultrastructural, and cytochemicalchanges. J Invest Dermatol, 1985, 84(1), 41–6.
[354] Aho, S; Mahoney, MG; Uitto, J. Plectin serves as an autoantigen in paraneoplastic pemphigus. J Invest Dermatol, 1999, 113, 422–3.
[355] Proby, C; Fujii, Y; Owaribe, K; Nishikawa, T; Amagai, M. Human autoantibodies against HD1/plectin in paraneoplastic pemphigus. J Invest Dermatol, 1999, 112, 153–6.
[356] Buijsrogge, JJ. Antiplectin autoantibodies insubepidermal blistering diseases. Br J Dermatol, 2009, 161, 762–71.
[357] Laffitte, E. Plectin, an unusual target antigen inbullous pemphigoid. Br J Dermatol, 2001, 144, 136–8.
[358] Buijsrogge, JJ. Inflammatory epidermolysis bullosa acquisita with coexistent IgA antibodies to plectin. Clin Exp Dermatol, 2005, 30, 531–4.
[359] Tirado-Sánchez, A; León-Dorantes, G. Treatment of pemphigus vulgaris. An overview in Mexico. Allergol Immunopathol (Madr), 2006, 34(1), 10-6.
[360] Beutner, EH; Jordan, RE. Demonstration of skin antibodiesin sera of pemphigus vulgaris patients bydirect immunofl uorescent staining. Proc Soc Exp Biol Med, 1964, 117, 505–10.
[361] Beutner, EH; Prigenzi, LS; Hale, W; Leme Cde, A; Bier, OG. Immunofluorescent studies of autoantibodies to intercellular areas of epithelia in Brazilian pemphigus foliaceus. Proc Soc Exp Biol Med, 1968, 127(1), 81–6.
[362] Eyre, RW; Stanley, JR. Identification of pemphigus vulgaris antigen extracted from normal human epidermis and comparison with pemphigus foliaceus antigen. J Clin Invest, 1988, 81(3), 807–12.
[363] Woo, TY; Hogan, VA; Patel, H; Anhalt, GJ; Labib, RS; Voorhees, JJ; et al. Specificity and inhibition of the epidermal cell detachment induced by pemphigus IgG in vitro. J Invest Dermatol, 1983, 81(1 Suppl), 115s–21.
[364] Hashimoto, K; Shafran, KM; Webber, PS; Lazarus, GS; Singer, KH. Anti-cell surface pemphigus autoantibody stimulates plasminogen activator activity of human epidermal cells. J Exp Med, 1983, 157, 259–72.
[365] Shimizu, A; Ishiko, A; Ota, T; Tsunoda, K; Amagai, M; Nishikawa. T. IgG binds to desmoglein 3 in desmosomesand causes a desmosomal split without keratinretraction in a pemphigus mouse model. J Invest Dermatol, 2004, 122(5), 1145–53.
[366] Esaki, C; Seishima, M; Yamada, T; Osada, K; Kitajima, Y. Pharmacologic evidence for involvement of phospholipase C in pemphigus IgG-induced inositol 1, 4, 5-trisphosphate generation, intracellular calcium increase, and plasminogen activator secretion in DJM-1 cells, asquamous cell carcinoma line. J Invest Dermatol, 1995, 105(3), 329–33.
[367] Osada, K; Seishima, M; Kitajima, Y. Pemphigus IgG activatesand translocates protein kinase C from the cytosolto the particulate/cytoskeleton fractions in human keratinocytes. J Invest Dermatol, 1997, 108(4), 482–7.
[368] Caldelari, R; de Bruin, A; Baumann, D; Suter, MM; Bierkamp, C; Balmer, V; et al. A central role for the armadillo protein plakoglobin in the autoimmune disease pemphigus vulgaris. J Cell Biol, 2001, 153(4), 823–34.
[369] Nguyen, VT; Ndoye, A; Shultz, LD; Pittelkow, MR; Grando, SA. Antibodies against keratinocyte antigensother than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions. J Clin Invest, 2000, 106(12), 1467–79 [comment].
[370] Nguyen, VT; Arredondo, J; Chernyavsky, AI; Kitajima, Y; Pittelkow, M; Grando, SA. Pemphigus vulgaris IgG and methylprednisolone exhibit reciprocal effects on keratinocytes. J Biol Chem, 2004, 279(3), 2135–46.
[371] Mascaro, Jr. JM; Espana, A; Liu, Z; et al. Mechanisms of acantholysis in pemphigus vulgaris: role of IgG valence. Clin Immunol Immunopathol, 1997, 85(1), 90–6.
[372] Payne, AS; Ishii, K; Kacir, S; et al. Genetic and functional characterization of human pemphigus vulgaris monoclonal autoantibodies isolated by phage display. J Clin Invest, 2005, 115(4), 888–99.
[373] Rogalla, T; Ehrnsperger, M; Preville, X; et al. Regulation of Hsp27 oligomerization, chaperone function, and protective activity against oxidative stress/tumor necrosis factor alpha by phosphorylation. J Biol Chem, 1999, 274(27), 18947–56.
[374] Lambert, H; Charette, SJ; Bernier, AF; Guimond, A; Landry, J. HSP27 multimerization mediated by phosphorylation- sensitive intermolecular interactions at the amino terminus. J Biol Chem, 1999, 274(14), 9378–85.
[375] Benndorf, R; Hayess, K; Ryazantsev, S; Wieske, M; Behlke, J; Lutsch, G. Phosphorylation and supramolecular organization of murine small heat shock proteinHSP25 abolish its actin polymerization-inhibitingactivity. J Biol Chem, 1994, 269(32), 20780–4.
[376] Geum, D; Son, GH; Kim, K. Phosphorylation-dependentcellular localization and thermoprotective role of heatshock protein 25 in hippocampal progenitor cells. J Biol Chem, 2002, 277(22), 19913–21.
[377] Panasenko, OO; Kim, MV; Marston, SB; Gusev, NB. Interaction of the small heat shock protein withmolecular mass 25 kDa (hsp25) with actin. Eur JBiochem/FEBS, 2003, 270(5), 892–901.
[378] Perng, MD; Cairns, L; van den IJssel, P; Prescott, A; Hutcheson, AM; Quinlan, RA. Intermediate filament interactions can be altered by HSP27 and alpha B crystallin. J Cell Sci, 1999, 112(Pt 13), 2099–112.
[379] Duverger, O; Paslaru, L; Morange, M. HSP25 is involved in two steps of the differentiation of PAM212 keratinocytes. J Biol Chem, 2004, 279(11), 10252–60.
[380] Lavoie, JN; Hickey, E; Weber, LA; Landry, J. Modulationof actin microfilament dynamics and fl uid phase pinocytosisby phosphorylation of heat shock protein 27. J Biol Chem, 1993, 268(32), 24210–4.
[381] Lavoie, JN; Lambert, H; Hickey, E; Weber, LA; Landry, J. Modulation of cellular thermoresistance and actin filament stability accompanies phosphorylationinduced changes in the oligomeric structure of heatshock protein 27. Mol Cell Biol, 1995, 15(1), 505–16.
[382] Guay, J; Lambert, H; Gingras-Breton, G; Lavoie, JN; Huot, J; Landry, J. Regulation of actin filament dynamics by p38 map kinase-mediated phosphorylation of heat shock protein 27. J Cell Sci, 1997, 110(Pt3), 357–68.
[383] Evgrafov, OV; Mersiyanova, I; Irobi, J; et al. Mutant small heat-shockprotein 27 causes axonal Charcot-Marie-Tooth disease and distal hereditary motor neuropathy. Nat Genet, 2004, 36(6), 602–6.
[384] Berkowitz, P; Hu, P; Warren, S; Liu, Z; Diaz, LA; Rubenstein, DS. p38MAPK inhibition prevents disease in pemphigus vulgaris mice. Proc Natl Acad Sci U S A, 2006, 103, 12855–60.
[385] Chernyavsky, AI; Arredondo, J; Kitajima, Y; Sato-Nagai, M; Grando, SA. Desmoglein versus non-desmoglein signaling in pemphigus acantholysis: characterization of novel signaling pathways downstream of pemphigus vulgaris antigens. J Biol Chem, 2007, 282(18), 13804–12.
[386] Kawasaki, Y; Aoyama, Y; Tsunoda, K; Amagai, M; Kitajima, Y. Pathogenic monoclonal antibody against desmoglein 3 augments desmoglein 3 and p38 MAPK phosphorylation in human squamous carcinoma cellline. Autoimmunity, 2006, 39(7), 587–90.
[387] Mao, X; Sano, Y; Park, JM; Payne, AS. p38 MAPK activation is downstream of the loss of intercellular adhesion in pemphigus vulgaris. J Biol Chem, 2011, 286(2), 1283–91.
[388] Waschke, J; Spindler, V; Bruggeman, P; Zillikens, D; Schmidt, G; Drenckhahn, D. Inhibition of Rho A activity causes pemphigus skin blistering. J Cell Biol, 2006, 175(5), 721–7.
[389] Delva, E; Jennings, JM; Calkins, CC; Kottke, MD; Faundez, V; Kowalczyk, AP. Pemphigus vulgaris IgG-induced desmoglein-3 endocytosis and desmosomal disassembly are mediated by a clathrin- and dynamin-independent mechanism. J Biol Chem, 2008, 283(26), 18303–13.
[390] Calkins, CC; Setzer, SV; Jennings, JM; Summers, S; Tsunoda, K; Amagai, M; et al. Desmoglein endocitosis and desmosome disassembly are coordinated responses to pemphigus autoantibodies. J Biol Chem, 2006, 281(11), 7623–34.
[391] Jolly, PS; Berkowitz, P; Bektas, M; Lee, HE; Chua, M; Diaz, LA; et al. p38MAPK signaling and desmoglein-3 internalization are linked events in pemphigus acantholysis. J Biol Chem, 2010, 285(12), 8936–41.
[392] Spindler, V; Vielmuth, F; Schmidt, E; Rubenstein, DS; Waschke, J. Protective endogenous cyclic adenosine 5′-monophosphate signaling triggered by pemphigusautoantibodies. J Immunol, 2010, 185(11), 6831–8.
[393] Rubenstein, DS; Werth, V; Strober, B; et al. Use of KC706 for the treatment of pemphigus vulgaris. pemphigus &rank=10.
[394] Murrell, D; Dick, S; Ahmed, A. Consensus statement on definitions of disease, end points, and therapeutic response for pemphigus. J Am Acad Dermatol, 2008, 58(6), 1043–6.
[395] Rosenbach, M; Murrell, DF; Bystryn, JC; Dulay, S; Dick, S; Fakharzadeh, S; et al. Reliability and convergent validity of two outcome instruments for pemphigus. J Invest Dermatol, 2009, 129(10), 2404–10.
[396] Muller, EJ; Hunziker, T; Suter, MM. Keratin intermediatefilament retraction is linked to plakoglobin dependent signaling in pemphigus vulgaris. J AmAcad Dermatol, 2007, 56(5), 890–1.
[397] Tsang, SM; Brown, L; Lin, K; Liu, L; Piper, K; O’Toole, EA; et al. Non-junctional human desmoglein 3 acts asan upstream regulator of Src in E-cadherin adhesion, a pathway possibly involved in the pathogenesis ofpemphigus vulgaris. J Pathol, 2012, 227(1), 81–93.
[398] Schulze, K; Galichet, A; Sayar, BS; Scothern, A; Howald, D; Zymann, H; et al. An adult passive transfer mousemodel to study desmoglein 3 signaling in pemphigus vulgaris. J Invest Dermatol, 2012, 132(2), 346–55.
[399] Spindler, V; Endlich, A; Hartlieb, E; Vielmuth, F; Schmidt, E; Waschke, J. The extent of desmoglein 3depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasalepidermal skin splitting? Am J Pathol, 2011, 179(4), 1905–16.
[400] Sanchez-Carpintero, I; Espana, A; Pelacho, B; LopezMoratalla, N; Rubenstein, DS; Diaz, LA; et al. In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades. Br J Dermatol, 2004, 151(3), 565–70.
[401] Pretel, M; Espana, A; Marquina, M; Pelacho, B; Lopez-Picazo, JM; Lopez-Zabalza, MJ. An imbalance in Akt/mTOR is involved in the apoptotic and acantholyticprocesses in a mouse model of pemphigus vulgaris. Exp Dermatol, 2009, 18(9), 771–80.
[402] Chernyavsky, AI; Arredondo, J; Piser, T; Karlsson, E; Grando, SA. Differential coupling of M1 muscarinic and alpha7 nicotinic receptors to inhibition of pemphigusacantholysis. J Biol Chem, 2008, 283(6), 3401–8.
[403] Seishima, M; Iwasaki-Bessho, Y; Itoh, Y; Nozawa, Y; Amagai, M; Kitajima, Y. Phosphatidylcholine-specificphospholipase C, but not phospholipase D, is involvedin pemphigus IgG-induced signal transduction. Arch Dermatol Res, 1999, 291(11), 606–13.
[404] Marconi, A; Atzei, P; Panza, C; et al. FLICE/caspase-8 activation triggers anoikis induced by beta1-integrin blockade in human keratinocytes. J Cell Sci, 2004, 117(Pt 24), 5815–23.
[405] Grando, SA; Bystryn, JC; Chernyavsky, AI; et al. Apoptolysis: anovel mechanism of skin blistering in pemphigus vulgarislinking the apoptotic pathways to basal cellshrinkage and suprabasal acantholysis. Exp Dermatol, 2009, 18(9), 764–70.
[406] Sarig, O; Bercovici, S; Zoller, L; et al. Population-specific associationbetween a polymorphic variant in ST18, encoding apro-apoptotic molecule, and pemphigus vulgaris. J Invest Dermatol, 2012, 132(7), 1798–805.
[407] Gazit, E; Lowenthal, R. The immunogenetics of pemphigus vulgaris. Autoimmun Rev, 2004, 4, 16–20.
[408] Yang, J; Siqueira, MF; Behl, Y; Alikhani, M; Graves, DT. The transcription factor ST18 regulates proapoptoticand proinflammatory gene expression in fibroblasts. FASEB J, 2008, 22(11), 3956–67.
[409] Pacheco-Tovar, MG; Avalos-Diaz, E; Vega-Memije, E; et al. The final destiny of acantholytic cells inpemphigus is Fas mediated. J Eur Acad DermatolVenereol, 2009, 23(6), 697–701.
[410] Frusic-Zlotkin, M; Raichenberg, D; Wang, X; David, M; Michel, B; Milner, Y. Apoptotic mechanism inpemphigus autoimmunoglobulins-induced acantholysis—possible involvement of the EGF receptor. Autoimmunity, 2006, 39(7), 563–75.
[411] Pelacho, B; Natal, C; Espana, A; Sanchez-Carpintero, I; Iraburu, MJ; Lopez-Zabalza, MJ. Pemphigus vulgarisautoantibodies induce apoptosis in HaCaT keratinocytes. FEBS Lett, 2004, 566(1–3), 6–10.
[412] Wang, X; Bregegere, F; Frusic-Zlotkin, M; Feinmesser, M; Michel, B; Milner, Y. Possible apoptotic mechanismin epidermal cell acantholysis induced by pemphigusvulgaris autoimmunoglobulins. Apoptosis, 2004, 9(2), 131–43.
[413] Wang, X; Bregegere, F; Soroka, Y; Frusic-Zlotkin, M; Milner, Y. Replicative senescence enhances apoptosis induced by pemphigus autoimmune antibodies inhuman keratinocytes. FEBS Lett, 2004, 567(2–3), 281–6.
[414] Pacheco-Tovar, D; Lopez-Luna, A; Herrera-Esparza, R; Avalos-Diaz, E. The caspase pathway as a posible therapeutic target in experimental pemphigus. Autoimmun Dis, 2011, 2011, 563091.
[415] Cirillo, N; Lanza, M; Femiano, F; et al. If pemphigus vulgaris IgG are thecause of acantholysis, new IgG-independent mechanisms are the concause. J Cell Physiol, 2007, 212(3), 563–7.
[416] D’Auria, L; Bonifati, C; Mussi, A; et al. Cytokines in the sera of patients with pemphigus vulgaris: interleukin-6 andtumour necrosis factor-alpha levels are significantlyincreased as compared to healthy subjects and correlate with disease activity. Eur Cytokine Netw, 1997, 8(4), 383–7.
[417] Siebra, MX; Santos, MA; Almeida, TL; Leite, AC; Cunha, FQ; Rocha, FA. Evidence for the participationof nitric oxide in pemphigus. Braz J Med Biol Res, 2006, 39(5), 671–5.
[418] Grando, SA; Glukhenky, BT; Drannik, GN; Kostromin, AP; Chernyavsky, AI. Cytotoxic proteasesin blister fluid of pemphigus and pemphigoidpatients. Int J Tissue React, 1989, 11(4), 195–201.
[419] Toosi, S; Habib, N; Torres, G; Reynolds, SR; Bystryn, JC. Serum levels of inhibitors of apoptotic proteins (IAPs) change with IVIg therapy in pemphigus. J Invest Dermatol, 2011, 131(11), 2327–9.
[420] Moravvej, H; Yousefi, M; Farrokhi, B; Mosaffa, N. Soluble Fas in pemphigus vulgaris. Arch Iran Med, 2011, 14(3), 200–1.
[421] Sayama, K; Yonehara, S; Watanabe, Y; Miki, Y. Expression of Fas antigen on keratinocytes in vivo and induction of apoptosis in cultured keratinocytes. JInvest Dermatol, 1994, 103(3), 330–4.
[422] Arredondo, J; Chernyavsky, AI; Karaouni, A; Grando, SA. Novel mechanisms of target cell death and survival and of therapeutic action of IVIg inpemphigus. Am J Pathol, 2005, 167(6), 1531–44.
[423] Orlov, MD; Chernyavsky, AI; Arredondo, J; Grando, SA. Synergistic actions of pemphigus vulgaris IgG, Fas-ligand and tumor necrosis factor-alpha duringinduction of basal cell shrinkage and acantholysis. Autoimmunity, 2006, 39(7), 557–62.
[424] Amagai, M; Tsunoda, K; Suzuki, H; Nishifuji, K; Koyasu, S; Nishikawa, T. Use of autoantigen- knockout mice in developing an active autoimmune disease model for pemphigus. J Clin Invest, 2000, 105(5), 625–31.
[425] Sinha, AA. The genetics of pemphigus. Dermatol Clin, 2011, 29(3), 381–91, vii.
[426] Tron, F; Gilbert, D; Joly, P; et al. Immunogenetics of pemphigus: an update. Autoimmunity, 2006, 39(7), 531–9.
[427] Todd, JA; Acha-Orbea, H; Bell, JI; et al. A molecularbasis for MHC class II—associated autoimmunity. Science, 1988, 240(4855), 1003–9.
[428] Scharf, SJ; Friedmann, A; Brautbar, C; et al. HLA classII allelic variation and susceptibility to pemphigusvulgaris. Proc Natl Acad Sci U S A, 1988, 85(10), 3504–8.
[429] Lee, E; Lendas, KA; Chow, S; et al. Disease relevantHLA class II alleles isolated by genotypic, haplotypic, and sequence analysis in North American Caucasianswith pemphigus vulgaris. Hum Immunol, 2006, 67(1–2), 125–39.
[430] Yan, L; Wang, JM; Zeng, K. Association between HLADRB1polymorphism and pemphigus vulgaris: A meta-analysis. Br J Dermatol, 2012, 167, 768–77.
[431] Bhanusali, D; Sachdev, A; Rahmanian, A; et al. HLAE*0103X is associated with susceptibility to pemphigus vulgaris. Exp Dermatol, 2013, 22(2), 108–12.
[432] Torzecka, JD; Narbutt, J; Sysa-Jedrzejowska, A; et al. Tumour necrosis factor-alpha polymorphism as one of the complex inherited factors in pemphigus. Mediators Inflamm, 2003, 12(5), 303–7.
[433] Martel, P; Loiseau, P; Joly, P; et al. Paraneoplastic pemphigus is associated with the DRB1* 03 allele. J Autoimmun, 2003, 20(1), 91–5.
[434] Liu, Q; Bu, D; Li, D; Zhu, X. Genotyping of HLA-I andHLA-II alleles in Chinese patients with paraneoplastic pemphigus. Br J Dermatol, 2008, 158(3), 587–91.
[435] Bordel-Gomez, MT; Sanchez-Estella, J; Yuste- Chaves, M; et al. Familial pemphigus vulgaris: immunogenetic study of HLA class II antigens. Actas Dermosifiliogr, 2006, 97, 509–13.
[436] Humbert, P; Dupond, JL; Vuitton, D; et al. Dermatological autoimmune diseases and the multiple autoimmunesyndromes. Acta Derm Venereol Suppl (Stockh), 1989, 148, 1–8.
[437] Mohan, MP; Ramesh, TC. Multiple autoimmune syndrome. Indian J Dermatol Venereol Leprol, 2003, 69, 298–9.
[438] Laskaris, G; Sklavounou, A; Stavrou, A; et al. Familial pemphigus vulgaris with oral manifestationsaffecting two Greek families. J Oral Pathol Med, 1989, 18, 49–53.
[439] Katzenelson, V; David, M; Zamir, R; et al. Familialpemphigus vulgaris. Dermatologica, 1990, 181, 48–50.
[440] Feinstein, A; Yorav, S; Movshovitz, M; et al. Pemphigus in families. Int J Dermatol, 1991, 30, 347–51.
[441] Stavropoulos, PG; Zarafonitis, G; Petridis, A; et al. Pemphigus vulgaris in two sisters. Acta Derm Venereol, 2001, 81, 149.
[442] Mashiah, J; Brenner, S. Medical pearl: first step in managing pemphigus—addressing the etiology. J Am Acad Dermatol, 2005, 53(4), 706–7.
[443] Brenner, S. PEMPHIGUS: an acronym for a diseasewith multiple etiologies. Skinmed, 2003, 2(3), 163–7.
[444] Brenner, S; Tur, E; Shapiro, J; et al. Pemphigus vulgaris: environmental factors. Occupational, behavioral, medical, and qualitative food frequencyquestionnaire. Int J Dermatol, 2001, 40(9), 562–9.
[445] Brenner, S; Bialy-Golan, A; Ruocco, V. Drug-induced pemphigus. Clin Dermatol, 1998, 16(3), 393–7.
[446] Brenner, S; Wolf, R; Ruocco, V. Contact pemphigus: a subgroup of induced pemphigus. Int J Dermatol, 1994, 33(12), 843–5.
[447] Goldberg, I; Kashman, Y; Brenner, S. The induction of pemphigus by phenol drugs. Int J Dermatol, 1999, 38(12), 888–92.
[448] Tamir, A; Ophir, J; Brenner, S. Pemphigus vulgaris triggered by emotional stress. Dermatol (Basel Switzerland), 1994, 189(2), 210.
[449] Jacobs, SE. Pemphigus erythematosus and ultraviolet light: a case report. Arch Dermatol, 1965, 91(2), 139.
[450] Brenner, S. Pemphigus and dietary factors. Dermatology, 1995, 190(3), 197–202.
[451] Tur, E; Brenner, S. Diet and pemphigus: in pursuit ofexogenous factors in pemphigus and fogo selvagem. Arch Dermatol, 1998, 134(11), 1406.
[452] Ruocco, V; Pisani, M. Induced pemphigus. Arch Dermatol Res, 1982, 274(1–2), 123–40.
[453] Wolf, R; Tamir, A; Brenner, S. Drug-induced versusdrug-triggered pemphigus. Dermatologica, 1991, 182(4), 207–10.
[454] Yamamoto, T; Takata-Michigami, M; Hisamatsu, Y; et al. A prospective analysis of anti-desmoglein antibody profiles in patients with rheumatoid arthritis treated with thiol compounds. J Dermatol Sci, 2010, 59(3), 170–5.
[455] Sebaratnam, DF; Martin, LK; Rubin, AI; et al. Reversible relapse of pemphigus foliaceus triggeredby topical imiquimod suggests that Toll-like receptor 7 inhibitors may be useful treatments for pemphigus. Clin Exp Dermatol, 2010, 36(1), 91–3.
[456] Tang, X; Zhang, X. Drug-induced pemphigus after six years of treatment with phenytoin and carbamazepine. Int J Dermatol, 2012, 51(4), 485–6.
[457] Valikhani, M; Kavusi, S; Chams-Davatchi, C; et al. Pemphigus and associated environmental factors: a casecontrolstudy. Clin Exp Dermatol, 2007, 32(3), 256–60.
[458] Valikhani, M; Kavusi, S; Chams-Davatchi, C; et al. Impact of smoking on pemphigus. Int J Dermatol, 2008, 47(6), 567–70.
[459] Mehta, JN; Martin, AG. A case of pemphigus vulgarisimproved by cigarette smoking. Arch Dermatol, 2000, 136(1), 15–7.
[460] Sullivan, TP; Elgart, GW; Kirsner, RS. Pemphigus and smoking. Int J Dermatol., 2002, 41(8), 528–30.
[461] Grando, SA; Dahl, MV. Nicotine and pemphigus. Arch Dermatol, 2000, 136(10), 1269.
[462] Arnson, Y; Shoenfeld, Y; Amital, H. Effects of tobacco smoke on immunity, inflammation and autoimmunity. J Autoimmun, 2010, 34(3), J258–65.
[463] Morell-Dubois, S; Carpentier, O; Cottencin, O; et al. Stressful life events and pemphigus. Dermatology, 2008, 216(2), 104–8.
[464] Bastuji-Garin, S; Turki, H; Mokhtar, I; et al. Possiblerelation of Tunisian pemphigus with traditional cosmetics: a multicenter case-control study. Am J Epidemiol, 2002, 155(3), 249–56.
[465] Micali, G; Nasca, MR; Musumeci, ML; Innocenzi, D. Postsurgical pemphigus. Dermatology, 1998, 197(2), 192–3.
[466] Tur, E; Brenner, S. Contributing exogenous factors inpemphigus. Int J Dermatol., 1997, 36(12), 888–93.
[467] Diaz, LA; Sampaio, SA; Rivitti, EA; et al. Endemicpemphigus foliaceus (fogo selvagem): II. Current andhistoric epidemiologic studies. J Invest Dermatol, 1989, 92(1), 4–12.
[468] Empinotti, JC; Aoki, V; Filgueira, A; et al. Clinical andserological follow-up studies of endemic pemphigus foliaceus (fogo selvagem) in Western Parana, Brazil (2001–2002). Br J Dermatol, 2006, 155(2), 446–50.
[469] Diaz, LA; Arteaga, LA; Hilario-Vargas, J; et al. Antidesmoglein-1 antibodies in onchocerciasis, leishmaniasis and Chagas disease suggest a possible etiologicallink to Fogo selvagem. J Invest Dermatol, 2004, 123(6), 1045–51.
[470] Qian, SX; Li, JY; Hong, M; Xu, W; Qiu HX. Nonhematological autoimmunity (glomerulosclerosis, paraneoplastic pemphigus and paraneoplasticneurological syndrome) in a patient with chronic lymphocyticleukemia: diagnosis, prognosis and management. Leuk Res, 2008, 33, 500–5.
[471] Moraes, ME; Fernandez-Vina, M; Lazaro, A; et al. An epitopein the third hypervariable region of the DRB1 gene is involved in the susceptibility to endemic pemphigus foliaceus (fogo selvagem) in three different Brazilian populations. Tissue Antigens, 1997, 49(1), 35–40.
[472] Bastuji-Garin, S; Souissi, R; Blum, L; et al. Comparativeepidemiology of pemphigus in Tunisia and France: unusual incidence of pemphigus foliaceus in young Tunisian women. J Invest Dermatol, 1995, 104(2), 302–5.
[473] Abida, O; Masmoudi, A; Rebai, A; et al. The familialfeature of Tunisian endemic pemphigus foliaceus. Br J Dermatol, 2009, 161(4), 951–3.
[474] Abida, O; Zitouni, M; Kallel-Sellami, M; et al. Tunisianendemic pemphigus foliaceus is associated with the HLA-DR3 gene: anti-desmoglein 1 antibody- positive healthy subjects bear protective alleles. Br J Dermatol, 2009, 161(3), 522–7.
[475] Joly, P; Mokhtar, I; Gilbert, D; et al. Immunoblot and immunoelectron microscopic analysis of endemic Tunisian pemphigus. Br J Dermatol, 1999, 140(1), 44–9.
[476] Kallel Sellami, M; Zitouni, M; Tombari, W; et al. Antidesmoglein-1 antibodies are prevalent in Tunisian patients with hydatidosis and leishmaniasis. Br J Dermatol, 2007, 156(3), 591–3.
[477] Zaraa, I; Boussoffara, T; Ben Ahmed, M; et al. Exposureto Phlebotomus papatasi and/or Leishmania major: possible etiologic link to Tunisian pemphigus. J Invest Dermatol, 2014, 132(2), 479–82.
[478] Lombardi, C; Borges, PC; Chaul, A; et al. Environmental risk factors in endemic pemphigus foliaceus (Fogo selvagem). ‘The Cooperative Group on Fogo Selvagem Research.’ J Invest Dermatol, 1992, 98, 847–850.
[479] Aoki, V; Sousa, JX; Jr, Diaz, LA. Pathogenesis of endemic pemphigus foliaceus. Dermatol Clin, 2011, 29, 413–418, viii.
[480] Wohl, Y; Brenner, S. Pemphigus in Israel _ an epidemiologic analysis of cases in search of risk factors. Women, 2003, 33, 60.
[481] Yazdanpanah, MJ; Ghayour-Mobarhan, M; Taji, A; et al. Serum zinc and copper status in Iranian patients with pemphigus vulgaris. Int J Dermatol, 2011, 50, 1343–1346.
[482] Meibodi, NT; Nahidi, Y; Mahmoudi, M; et al. Evaluation of coexistence of the human herpesvirus type 8 (HHV-8) in fection and pemphigus. Int J Dermatol, 2010, 49, 780–783.
[483] Fallahzadeh, MK; Lashkarizadeh, H; Kamali-Sarvestani, E; Namazi, MR. Elevation of serum prolactin levels in patients with pemphigus vulgaris: a novel finding with practical implications. J Am Acad Dermatol, 2010, 62, 1071–1072.
[484] Wohl, Y; Dreiher, J; Cohen, AD. Pemphigus and dyslipidaemia: a case–control study. Br J Dermatol, 2009, 161, 1418–1420.
[485] Da Cunha, SF; dos Santos, VM; Monteiro, JP; et al. Serum lipids of pemphigus foliaceus patients on long-term glucocorticoid therapy. Rev Soc Bras Med Trop, 2003, 36, 1–4.
[486] Daneshpazhooh, M; Behjati, J; Hashemi, P; et al. Thyroid autoimmunity and pemphigus vulgaris: is there a significant association? J Am Acad Dermatol, 2010, 62, 349–351.
[487] Kacar, N; Cevahir, N; Demirkan, N; Sanli, B. The investigation of the possible relationship between Coxsackie viruses and pemphigus. Int J Dermatol, 2014, 53, 312–315.
[488] Mozafari, N; Robati, RM; Younespour, S. Serum leptin levels in pemphigus: a case control study. Biomed Res Int, 2014, 2014, 5.
[489] Shapira, Y; Agmon-Levin, N; Shoenfeld, Y. Definingand analyzing geoepidemiology and human autoimmunity. J Autoimmun, 2010, 34(3), J168–77.
[490] Arbuckle, MR; McClain, MT; Rubertone, MV; et al. Development of autoantibodies before the clinicalonset of systemic lupus erythematosus. N Engl J Med, 2003, 349(16), 1526–33.
[491] Ortega Loayza, AG; Ramos, W; Elgart, G; et al. Antibodies against desmoglein 1 in healthy subjectsin endemic and nonendemic areas of pemphigus foliaceus(fogo selvagem) in Peru. Int J Dermatol, 2006, 45(5), 538–42.
[492] Amagai, M; Tsunoda, K; Zillikens, D; Nagai, T; Nishikawa, T. The clinical phenotype of pemphigus isdefined by the anti-desmoglein autoantibody profile. J Am Acad Dermatol, 1999, 40(2 Pt 1), 167–70.
[493] Aboobaker, J; Wojnarowska, FT; Bhogal, B; Black, MM. Chronic bullous dermatosis of childhood—clinical and immunological features seen in Africanpatients. Clin Exp Dermatol, 1991, 16(3), 160–4.
[494] Baican, A; Baican, C; Chiriac, G; et al. Pemphigus vulgarisis the most common autoimmune bullous diseasein northwestern Romania. Int J Dermatol, 2010, 49(7), 768–74.
[495] Chams-Davatchi, C; Valikhani, M; Daneshpazhooh, M; et al. Pemphigus: analysis of 1209 cases. Int J Dermatol, 2005, 44(6), 470–6.
[496] Hahn, K; Kippes, W; Amagai, M; Rzany, B; Brocker, EB; Zillikens, D. Clinical aspects and immunopathologyin 48 patients with pemphigus. Hautarzt, 2000, 51(9), 670–7.
[497] Kumar, KA. Incidence of pemphigus in Thrissur district, south India. Indian J Dermatol Venereol Leprol, 2008, 74(4), 349–51.
[498] Salmanpour, R; Shahkar, H; Namazi, MR; Rahman-Shenas, MR. Epidemiology of pemphigus in southwestern Iran: a 10-year retrospective study (1991–2000). Int J Dermatol, 2006, 45(2), 103–5.
[499] Mahe, A; Flageul, B; Cisse, I; Keita, S; Bobin, P. Pemphigus in Mali: a study of 30 cases. Br J Dermatol, 1996, 134(1), 114–9.
[500] Micali, G; Musumeci, ML; Nasca, MR. Epidemiologicanalysis and clinical course of 84 consecutive cases ofpemphigus in eastern Sicily. Int J Dermatol, 1998, 37(3), 197–200.
[501] Tallab, T; Joharji, H; Bahamdan, K; Karkashan, E; Mourad, M; Ibrahim, K. The incidence of pemphigusin the southern region of Saudi Arabia. Int J Dermatol, 2001, 40(9), 570–2.
[502] Uzun, S; Durdu, M; Akman, A; et al. Pemphigus in theMediterranean region of Turkey: a study of 148 cases. Int J Dermatol., 2006, 45(5), 523–8.
[503] V’Lckova-Laskoska, MT; Laskoski, DS; Kamberova, S; Caca-Biljanovska, N; Volckova, N. Epidemiology ofpemphigus in Macedonia: a 15-year retrospectivestudy (1990–2004). Int J Dermatol, 2007, 46(3), 253–8.
[504] Amin, MN; Islam, AZ. Clinical, histologic and immunologicfeatures of pemphigus in Bangladesh. Int J Dermatol, 2006, 45(11), 1317–8.
[505] Krain, LS. Pemphigus. Epidemiologic and survivalcharacteristics of 59 patients, 1955–1973. Arch Dermatol, 1974, 110(6), 862–5.
[506] Zaraa, I; Kerkeni, N; Ishak, F; et al. Spectrum of autoimmuneblistering dermatoses in Tunisia: an 11-year study and a review of the literature. Int J Dermatol, 2011, 50(8), 939–44.
[507] Golusin, Z; Poljacki, M; Jovanovic, M; Ethuran, V; Stojanovic, S; Rajic, N. Some epidemiological features of pemphigus chronicus in south Vojvodina: a 12-yearretrospective study. Int J Dermatol, 2005, 44(9), 792–3.
[508] Goncalves, GA; Brito, MM; Salathiel, AM; Ferraz, TS; Alves, D; Roselino, AM. Incidence of pemphigus vulgaris exceeds that of pemphigus foliaceus in a regionwhere pemphigus foliaceus is endemic: analysis of a21-year historical series. An Bras Dermatol, 2011, 86(6), 1109–12.
[509] Ahmed, AR; et al. Major histocompatibility complexhaplotype studies in Ashkenazi Jewish patientswith pemphigus vulgaris. Proc Natl Acad Sci U S A., 1990, 87(19), 7658–62.
[510] Hietanen, J; Salo, OP. Pemphigus: an epidemiological study of patients treated in Finnish hospitals between 1969 and 1978. Acta Derm Venereol, 1982, 62, 491–496.
[511] Marazza, G; Pham, HC; Scharer, L; et al. Incidence of bullous pemphigoid and pemphigus in Switzerland: a 2-year prospective study. Br J Dermatol, 2009, 161(4), 861–8.
[512] Michailidou, EZ; Belazi, MA; Markopoulos, AK; Tsatsos, MI; Mourellou, ON; Antoniades, DZ. Epidemiologic survey of pemphigus vulgaris with oralmanifestations in northern Greece: retrospective studyof 129 patients. Int J Dermatol, 2007, 46(4), 356–61.
[513] Pisanti, S; Sharav, Y; Kaufman, E; Posner, LN. Pemphigus vulgaris: incidence in Jews of differentethnic groups, according to age, sex, and initial lesion. Oral Surg Oral Med Oral Pathol, 1974, 38(3), 382–7.
[514] Simon, DG; Krutchkoff, D; Kaslow, RA; Zarbo, R. Pemphigus in Hartford County, Connecticut, from 1972 to 1977. Arch Dermatol, 1980, 116(9), 1035–7.
[515] Thomas, CW; et al. Selective inhibition of inflammatory gene expression in activated T lymphocytes: amechanism of immune suppression by thiopurines. J Pharmacol Exp Ther, 2005, 312, 537–45.
[516] Adam, BA. Bullous diseases in Malaysia, epidemiology and natural history. Int J Dermatol, 1992, 31(1), 42–5.
[517] Morini, JP; Jomaa, B; Gorgi, Y; et al. Pemphigus foliaceus in young women. An endemic focus in the Sousse area of Tunisia. Arch Dermatol, 1993, 129(1), 69–73.
[518] Tsankov, N; Vassileva, S; Kamarashev, J; Kazandjieva, J; Kuzeva, V. Epidemiology of pemphigus in Sofia, Bulgaria. A 16-year retrospective study (1980–1995). Int J Dermatol, 2000, 39(2), 104–8.
[519] Bertram, F; Brocker, EB; Zillikens, D; Schmidt, E. Prospective analysis of the incidence of autoimmunebullous disorders in Lower Franconia, Germany. J Dtsch Dermatol Ges, 2009, 7(5), 434–40.
[520] Hahn-Ristic, K; Rzany, B; Amagai, M; Brocker, EB; Zillikens, D. Increased incidence of pemphigus vulgaris in southern Europeans living in Germany comparedwith native Germans. J Eur Acad Dermatol Venereol, 2002, 16(1), 68–71.
[521] Bozdag, K; Bilgin, I. Epidemiology of pemphigus inthe western region of Turkey: retrospective analysis of 87 patients. Cutan Ocul Toxicol, 2012, 31, 280–5.
[522] Langan, SM; Smeeth, L; Hubbard, R; Fleming, KM; Smith, CJ; West, J. Bullous pemphigoid and pemphigusvulgaris—incidence and mortality in the UK: population based cohort study. BMJ, 2008, 337(7662), 160.
[523] Huang, YH; Kuo, CF; Chen, YH; Yang, YW. Incidence, mortality, and causes of death of patients with pemphigusin Taiwan: a nationwide population-basedstudy. J Invest Dermatol, 2012, 132(1), 92–7.
[524] Marinovic, B; Lipozencic, J; Jukic, IL. Autoimmuneblistering diseases: incidence and treatment in Croatia. Dermatol Clin, 2011, 29(4), 677–9.
[525] Groves, RW; Bhogal, B; Taghipour, K; Caposciutti, P; Saha, M. Bullous pemphigoid: is the incidence ofpemphigoid really increasing? BMJ, 2008, 337, a1138.
[526] Wilson, C. Pemphigus in Oxford, UK, and NewDelhi, India; a comparative study of disease characteristics and HLA antigens. Dermatology, 1994, 189(1), 108–10.
[527] Bickle, KM; Roark, TR; Hsu, S. Autoimmune bullous dermatoses: a review. Am Fam Physician, 2002, 65(9), 1861–82.
[528] Mutasim, DF. Immunobullous diseases. J Am Acad Dermatol, 2005, 52(6), 1029–43.
[529] Chmurova, N; Svecova, D. Pemphigus vulgaris: a 11-year review. Bratisl Lek Listy, 2009, 110(8), 500–3.
[530] Gorsky, M; Raviv, M; Raviv, E. Pemphigus vulgaris in adolescence: a case presentation and review of the literature. Oral Surg Oral Med Oral Pathol, 1994, 77(6), 620–2.
[531] Baican, A; Chiorean, R; Leucuta, DC; Baican, C; Danescu, S; Ciuce, D; Sitaru, C. Prediction of survival for patients with pemphigus vulgaris and pemphigus foliaceus: a retrospective cohort study. Orphanet J Rare Dis, 2015, 10, 48.
[532] Saha, M; Bhogal, B; Black, MM; Cooper, D; Vaughan, RW; Groves, RW. Prognostic factors in pemphigus vulgaris and pemphigus foliaceus. Br J Dermatol, 2014, 170(1), 116-22.
[533] Risser, J; Lewis, K; Weinstock, MA. Mortality of bullous skin disorders from 1979 through 2002 in theUnited States. Arch Dermatol, 2009, 145(9), 1005–8.
[534] Ahmed, AR; Moy, R. Death in pemphigus. J Am Acad Dermatol, 1982, 7(2), 221–8.
[535] Leshem, YA; Katzenelson, V; Yosipovitch, G; David, M; Mimouni, D. Autoimmune diseases in patients with pemphigus and their first-degree relatives. Int JDermatol, 2011, 50(7), 827–31.
[536] Wohl, Y; Dreiher, J; Cohen, AD. Pemphigus and osteoporosis: a case-control study. Arch Dermatol, 2010, 146(10), 1126–31.
[537] Tee, SI; Yosipovitch, G; Chan, YC; et al. Prevention of glucocorticoid-induced osteoporosis in immunobullous diseases with alendronate: a randomized, double blind, placebo-controlled study. Arch Dermatol, 2012, 148(3), 307–14.
[538] Diaz, LA; Sampaio, SA; Rivitti, EA; et al. Endemicpemphigus foliaceus (fogo selvagem). I. Clinical featuresand immunopathology. J Am Acad Dermatol, 1989, 20(4), 657–69.
[539] Robledo, MA; Prada, S; Jaramillo, D; Leon, W. South American pemphigus foliaceus: study of an epidemicin El Bagre and Nechi, Colombia 1982 to 1986. Br J Dermatol, 1988, 118(6), 737–44.
[540] Abreu-Velez, AM; Hashimoto, T; Bollag, WB; et al. Aunique form of endemic pemphigus in northern Colombia. J Am Acad Dermatol, 2003, 49(4), 599–608.
[541] Abreu-Velez, AM; Howard, MS; Jiao, Z; et al. Cardiac autoantibodies from patients affected by a new variant of endemic pemphigus foliaceus in Colombia, SouthAmerica. J Clin Immunol, 2011, 31(6), 985–97.
[542] Abreu-Velez, AM; Howard, MS; Yi, H; Gao, W; Hashimoto, T; Grossniklaus, HE. Neural system antigensare recognized by autoantibodies from patients affected by a new variant of endemic pemphigus foliaceusin Colombia. J Clin Immunol, 2011, 31(3), 356–68.
[543] Zimmermann, J; Bahmer, F; Rose, C; Zillikens, D; Schmidt, E. Clinical and immunopathological spectrumof paraneoplastic pemphigus. J Dtsch Dermatol Ges, 2010, 8(8), 598–605.
[544] Leger, S; Picard, D; Ingen-Housz-Oro, S; et al. Prognostic factors of paraneoplastic pemphigus. Arch Dermatol, 2012, 16, 1–8.
[545] Joly, P; Richard, C; Gilbert, D; et al. Sensitivity and specificity of clinical, histologic, and immunologic features in the diagnosis of paraneoplastic pemphigus. J Am Acad Dermatol, 2000, 43(4), 619–26.
[546] Ohyama, M; Amagai, M; Hashimoto, T; Nousari, HC;Anhalt, GJ; Nishikawa, T. Clinical phenotype and antidesmoglein autoantibody profile in paraneoplastic pemphigus. J Am Acad Dermatol, 2001, 44(4), 593–8.
[547] Huilgol, SC; Black, MM. Management of the immunobullous disorders. II. Pemphigus. Clin Exp Dermatol, 1995, 20(4), 283–93.
[548] Bédane, C; Prost, C; Thomine, E; et al. Binding of autoantibodiesis not restricted to desmosomes in pemphigus vulgaris, comparison of 14 cases of pemphigus vulgaris and 10 cases of pemphigus foliaceus studied by western immunoblot and immunoelectron microscopy. Arch Dermatol Res, 1996, 288(7), 343–52.
[549] Meurer, M. Oral pemphigus vulgaris: a report often cases. Arch Dermatol, 1977, 113(11), 1520.
[550] Sirois, DA. Diagnostic patterns and delays inpemphigus vulgaris: experience with 99 patients. Arch Dermatol, 2000, 136(12), 1569.
[551] Goldberg, NS; Weiss, SS. Pemphigus vulgaris of the esophagus in women. J Am Acad Dermatol, 1989, 21(5), 1115–8.
[552] Baykal, H. Severe eye involvement in pemphigus vulgaris. Ophthalmologe, 1995, 92(6), 854.
[553] Hodak, E. Conjunctival involvement in pemphigus vulgaris: a clinical, histopathological and immunofluorescence study. Br J Dermatol, 1990, 123(5), 615–20.
[554] Batta, K; Munday, P; Tatnall, F. Pemphigus vulgaris localized to the vagina presenting as chronic vaginal discharge. Br J Dermatol, 1999, 140(5), 945–7.
[555] Chan, E. Pemphigus vulgaris of the cervix andupper vaginal vault: a cause of atypical Papanicolaou smears. Arch Dermatol, 1998, 134(11), 1485.
[556] Malik, M; Ahmed, AR. Involvement of the femalegenital tract in pemphigus vulgaris. Obstet Gynecol, 2005, 106(5, Part 1), 1005.
[557] Malik, M; El Tal, AE; Ahmed, AR. Anal involvementin pemphigus vulgaris. Dis Colon Rectum, 2006, 49(4), 500–6.
[558] Hale, EK; Bystryn, JC. Laryngeal and nasal involvement in pemphigus vulgaris. J Am Acad Dermatol, 2001, 44(4), 609–11.
[559] Sami, N; Ahmed, AR. Penile pemphigus. Arch Dermatol, 2001, 137(6), 756.
[560] Korman, N. Pemphigus. J Am Acad Dermatol, 1988, 18(6), 1219–38.
[561] Udey, MC; Stanley, JR. Pemphigus—diseases of antidesmosomal autoimmunity. JAMA, 1999, 282(6), 572–6.
[562] Yesudian, PD. Postpemphigus acanthomata: a sign of clinical activity? Int J Dermatol, 1997, 36(3), 194–6.
[563] Yoshida, K. Cutaneous type pemphigus vulgaris: a rare clinical phenotype of pemphigus. J Am Acad Dermatol, 2005, 52(5), 839–45.
[564] Kolivras, A; Gheeraert, P; Andre, J. Nail destructionin pemphigus vulgaris. Dermatology, 2003, 206(4), 351–2.
[565] Berker, D. Pemphigus associated with naildystrophy. Br J Dermatol., 1993, 129(4), 461–4.
[566] Robinson, ND; Hashimoto, T; Amagai, M; Chan, LS. The new pemphigus variants. J Am Acad Dermatol, 1999, 40, 649–71.
[567] Santi, CG; Maruta, CW; Aoki, V; et al. Pemphigus herpetiformisis a rare clinical expression of non-endemicpemphigus foliaceus: fogo selvagem and pemphigusvulgaris. J Am Acad Dermatol, 1996, 34(1), 40–6.
[568] Yamamoto, S; Kanekura, T; Gushi, A; et al. A case oflocalized pemphigus foliaceus. J Dermatol, 1996, 23, 893–5.
[569] Nousari, HC; Moresi, M; Klapper, M; Anhalt GJ. Nonendemic pemphigus foliaceus presenting as fatal bullous exfoliative erythroderma. Cutis, 2001, 67, 251–2.
[570] Auad, A; Castro, RM; Fraga, S; et al. The treatment of Brazilian pemphigus foliaceus (fogo selvagem). Int J Dermatol, 1970, 9(2), 130–6.
[571] Meyer, N; Misery, L. Geoepidemiologic considerations of auto-immune pemphigus. Autoimmun Rev, 2010, 9, A379–82.
[572] Penas, PF; Buezo, GF; Carvajal, I; et al. D-Penicillamine-induced pemphigus foliaceus with autoantibodies todesmoglein-1 in a patient with mixed connective tissue disease. J Am Acad Dermatol, 1997, 37, 121–3.
[573] Ong, CS; Cook, N; Lee, S. Drug-related pemphigus andangiotensin converting enzyme inhibitors. Australas J Dermatol, 2000, 41, 242–6.
[574] Lee, CW; Lim, JH; Kang, HJ. Pemphigus foliaceus induced by rifampicin. Br J Dermatol, 1984, 111, 619–22.
[575] Lin, R; Ladd, Jr. DJ; Powell, DJ; Way, BV. Localizedpemphigus foliaceus induced by topical imiquimodtreatment. Arch Dermatol, 2004, 140(7), 889–90.
[576] Cram, DL; Winkelmann, RK. Ultraviolet-induced acantholysis in pemphigus. Arch Dermatol, 1965, 92, 7–13.
[577] Low, GJ; Keeling, JH. Ionizing radiation-induced pemphigus: case presentations and literature review. Arch Dermatol, 1990, 126, 1319–23.
[578] Korman, NJ; Stanley, JR; Woodley, DT. Coexistence ofpemphigus foliaceus and bullous pemphigoid. Arch Dermatol, 1991, 127, 387–90.
[579] Ishiko, A; Hashimoto, T; Shimizu, H; et al. Combined features of pemphigus foliaceus and bullous pemphigoid: immunoblot and immunoelectron microscopic studies. Arch Dermatol, 1995, 131, 732–4.
[580] Imamura, S; Takigawa, M; Ikai, K; et al. Pemphigusfoliaceus, myasthenia gravis, thymoma and red cellaplasia. Clin Exp Dermatol, 1978, 3, 285–91.
[581] Ng, PP; Ng, SK; Chng, HH. Pemphigus foliaceus andoral lichen planus in a patient with systemic lupus erythematosus and thymoma. Clin Exp Dermatol, 1998, 23, 181–4.
[582] Kwon, HH; Kwon, IH; Chung, JH; Youn, JI. Pemphigus foliaceus associated with psoriasis during the course of narrow-band UVB therapy: a simple coincidence? Ann Dermatol, 2011, 23(3), S281–4.
[583] Cowley, NC; Neill, SM; Staughton, RCD. Pemphigus foliaceus and non-Hodgkin’s lymphoma. Int J Dermatol, 1994, 33, 510–1.
[584] Rybojad, M; Leblanc, T; Flageul, B; et al. Paraneoplasticpemphigus in a child with a T-cell lymphoblastic lymphoma. Br J Dermatol, 1993, 128, 418–22.
[585] Ota, M; Sato-Matsumura, KC; Matsumura, T; et al. Pemphigus foliaceus and figurate erythema in a patient with prostate cancer. Br J Dermatol, 2000, 142, 816–8.
[586] Inaoki, M; Kodera, M; Fujimoto, A; Nousari, H; Anhalt, G; Takehara, K. Paraneoplastic pemphigus withoutantidesmoglein 3 or antidesmoglein 1 autoantibodies. Br J Dermatol., 2001, 144(3), 610–3.
[587] Kawana, S; Hashimoto, T; Nishikawa, T; et al. Changesin clinical features, histologic findings, and antigen profiles with development of pemphigus foliaceus from pemphigus vulgaris. Arch Dermatol, 1994, 130, 1534–8.
[588] Tsuji, Y; Kawashima, T; Yokota, K; et al. Clinical andserological transition from pemphigus vulgaris topemphigus foliaceus demonstrated by desmoglein ELISA system. Arch Dermatol, 2002, 138, 95–6.
[589] Ishii, K; Amagai, M; Ohata, Y; et al. Development of pemphigus vulgaris in a patient with pemphigus foliaceus: antidesmoglein antibody profile shift confirmedby enzyme-linked immunosorbent assay. J Am Acad Dermatol, 2000, 42, 859–61.
[590] Maeda, JY; Moura, AK; Maruta, CW; et al. Changes inthe autoimmune blistering response: a clinical andimmunopathological shift from pemphigus foliaceusto bullous pemphigoid. Clin Exp Dermatol, 2006, 31(5), 653–5.
[591] Amerian, ML; Ahmed, AR. Pemphigus erythematosus: presentation of four cases and review of literature. J Am Acad Derm, 1984, 10(2), 215–22.
[592] Bruckner, N; Katz, RA; Hood, AF. Pemphigus foliaceus resembling eruptive seborrheic keratoses. Arch Dermatol, 1980, 116, 815–6.
[593] Kahana, M; Trau, H; Schewach-Millet, M; et al. Pemphigusfoliaceus presenting as multiple giant seborrheic keratoses. J Am Acad Dermatol, 1984, 11, 299–300.
[594] Metry, DW; Hebert, AA; Jordon, RE. Nonendemic pemphigus foliaceus in children. J Am Acad Dermatol, 2002, 46, 419–22.
[595] Ohata, C; Akamatsu, K; Imai, N; Sumimura, Y. Localized pemphigus foliaceus exclusively involving the follicular infundibulum: a novel peau d’orangeappearance. Eur J Dermatol, 2011, 21, 392–5.
[596] Nagao, K; Tanikawa, A; Yamamoto, N; Amagai, M. Declineof anti-desmoglein 1 IgG ELISA scores by withdrawal of D-penicillamine in drug-induced pemphigus foliaceus. Clin Exp Dermatol, 2005, 30(1), 43–5.
[597] Camisa, C; Helm, TN. Paraneoplastic pemphigus is adistinct neoplasia-induced autoimmune disease. Arch Dermatol, 1993, 129(7), 883.
[598] Nguyen, V; Ndoye, A; Bassler, K; Shultz, L; Shields, M; Ruben, B; et al. Classification, clinical manifestations, and immunopathological mechanisms of the epithelialvariant of paraneoplastic autoimmune multiorgan syndrome: a reappraisal of paraneoplastic pemphigus. Arch Dermatol, 2001, 137(2), 193.
[599] Kaplan, I; Hodak, E; Ackerman, L; Mimouni, D; Anhalt, GJ; Calderon, S. Neoplasms associated with paraneoplasticpemphigus, a review with emphasis on nonhematologicmalignancy and oral mucosalmanifestations. Oral Oncol, 2004, 40(6), 553–62.
[600] Wang, J; Zhu, X; Li, R; Tu, P; Wang, R; Zhang, L; et al. Paraneoplastic pemphigus associated with Castlemantumor: a commonly reported subtype of paraneoplasticpemphigus in China. Arch Dermatol, 2005, 141(10), 1285.
[601] Lemon, M; Weston, W; Huff, J. Childhood paraneoplasticpemphigus associated with Castleman’s tumour. Br J Dermatol, 1997, 136(1), 115–7.
[602] Zhang, J; Qiao Q; Chen, X; et al. Improved outcomes after complete resection ofunderlying tumors for patients with paraneoplasticpemphigus: a single-center experience of 22 cases. J Cancer Res Clin Oncol, 2011, 137(2), 229–34.
[603] Lee, IJ; Kim, SC; Kim, HS; et al. Paraneoplastic pemphigus associated with follicular dendritic cell sarcoma arising from Castleman’s tumor. J Am Acad Dermatol, 1999, 40(2), 294–7.
[604] Wang, J; Bu, D; Li, T; Zheng, R; Zhang, B; Chen, X; et al. Autoantibody production from a thymoma and a folliculardendritic cell sarcoma associated with paraneoplastic pemphigus. Br J Dermatol, 2005, 153(3), 558–64.
[605] Choi, PCL; To, K; Lai, FMM; Lee, TW; Yim, APC; Chan, JKC. Follicular dendritic cell sarcoma of the neck. Cancer, 2000, 89(3), 664–72.
[606] Kim, WY; Kim, H; Jeon, YK; Kim, CW. Follicular dendriticcell sarcoma with immature T-cell proliferation. Hum Pathol, 2010, 41(1), 129–33.
[607] Haeryfar, S; Hickman, HD; Irvine, KR; Tscharke, DC; Bennink, JR; Yewdell, JW. Terminal deoxynucleotidyltransferase establishes and broadens antiviral CD8+ Tcell immunodominance hierarchies. J Immunol, 2008, 181(1), 649.
[608] Kedzierska, K; Thomas, PG; Venturi, V; Davenport, MP; Doherty, PC; Turner, SJ; et al. Terminal deoxynucleotidyltransferase is required for the establishment of privatevirus-specific CD8+ T-cell receptor repertoires andfacilitates optimal CTL responses. J Immunol, 2008, 181(4), 2556.
[609] Rosen, D; Lee, JH; Cuttitta, F; Rafiqi, F; Degan, S; Sunday, ME. Accelerated thymic maturation and autoreactiveT cells in bronchopulmonary dysplasia. Am JRespir Crit Care Med, 2006, 174(1), 75.
[610] Wang, L; Bu, D; Yang, Y; Chen, X; Zhu, X. Castleman’stumours and production of autoantibody in paraneoplasticpemphigus. Lancet, 2004, 363(9408), 525–31.
[611] Sklavounou, A; Laskaris, G. Paraneoplastic pemphigus: a review. Oral Oncol, 1998, 34(6), 437–40.
[612] Fullerton, S; Woodley, DT; Smoller, BR; Anhalt, GJ. Paraneoplastic pemphigus with autoantibody depositionin bronchial epithelium after autologous bonemarrow transplantation. JAMA, 1992, 267(11), 1500.
[613] Fried, R; Lynfield, Y; Vitale, P; Anhalt, G. Paraneoplasticpemphigus appearing as bullous pemphigoid-like eruption after palliative radiation therapy. J Am Acad Dermatol, 1993, 29(5), 815–7.
[614] Hashimoto, T; Maciejewskab, B; Amagaid, M; Anhalte, GJ; Jablonskaa S. Paraneoplastic pemphigus associated with Castleman tumor, myasthenia gravis and bronchiolitis obliterans. J Am Acad Dermatol, 1999, 41(3), 393–400.
[615] Powell, A; Albert, S; Oyama, N; Sakuma‐Oyama, Y; Bhogal, B; Black M. Paraneoplastic pemphigus secondaryto fludarabine evolving into unusual oral pemphigus vegetans. J Eur Acad Dermatol Venereol, 2004, 18(3), 360–4.
[616] Sapadin, A; Anhalt, G. Paraneoplastic pemphigus with a pemphigus vegetans-like plaque as the only cutaneous manifestation. J Am Acad Dermatol., 1998, 39(5), 867–71.
[617] Camisa, C; Helm, TN; Liu, YC; et al. Paraneoplastic pemphigus: a report of three cases including one long-term survivor. J Am Acad Dermatol, 1992, 27(4), 547–53.
[618] Wadhera, A; Maverakis, E; Mitsiades, N; Lara, PN; Fung, MA; Lynch, PJ. Thymoma-associated multiorgan autoimmunity: a graft-versus-host–like disease. J Am Acad Dermatol, 2007, 57(4), 683–9.
[619] Cummins, DL; Mimouni, D; Tzu, J; Owens, N; Anhalt, GJ; Meyerle, JH. Lichenoid paraneoplastic pemphigusin the absence of detectable antibodies. J Am Acad Dermatol, 2007, 56(1), 153–9.
[620] Preisz, K; Horvath, A; Sardy, M; et al. Exacerbation of paraneoplastic pemphigus by cyclophosphamide treatment: detection of novel autoantigens and bronchial autoantibodies. Br J Dermatol, 2004, 150(5), 1018–24.
[621] Czernik, A; Camilleri, M; Pittelkow, MR; Grando, SA. Paraneoplastic autoimmune multiorgan syndrome: 20 years after. Int J Dermatol, 2011, 50(8), 905–14.
[622] Wakahara, M; Kiyohara, T; Kumakiri, M; et al. Paraneoplastic pemphigus with wide spread mucosal involvement. Acta DermVenereol, 2005, 85(6), 530.
[623] Miida, H; Kazama, T; Inomata, N; et al. Severe gastrointestinal involvement inparaneoplastic pemphigus. Eur J Dermatol, 2006, 16, 420–2.
[624] Nousari, HC; Brodsky, RA; Jones, RJ; Grever, MR; Anhalt, GJ. Immunablative high-dose cyclophosphamide without stem cell rescue in paraneoplastic pemphigus: report of a case and review of this new therapyfor severe autoimmune disease. J Am Acad Dermatol, 1999, 40, 750–4.
[625] Qian, SX; Li, JY; Hong, M; Xu, W; Qiu, H. Non hematological autoimmunity (glomerulosclerosis; paraneoplastic pemphigus and paraneoplastic neurological syndrome) in a patient with chronic lymphocyticleukemia: diagnosis, prognosis and management. Leuk Res, 2009, 33(3), 500.
[626] Hayanga, AJ; Lee, TM; Pannucci, CJ; et al. Paraneoplastic pemphigus in aburn intensive care unit: case report and review of the literature. J Burn Care Res, 2010, 31(5), 826.
[627] Woodrow, JP; Shlobin, OA; Barnett, SD; Burton, N; Nathan, SD. Comparison of bronchiolitis obliterans syndrome to other forms of chronic lung allograftdys function after lung transplantation. J Heart Lung Transplant, 2010, 29(10), 1159–64.
[628] Maldonado, F; Pittelkow, MR; Ryu, JH. Constrictivebronchiolitis associated with paraneoplastic autoimmunemulti-organ syndrome. Respirology, 2009, 14(1), 129–33.
[629] Wang, J; Bu, D; Zhu, X. Immunoglobulin variable region gene analysis to the autoantibody-secreting Bcells from tumors in association with paraneoplasticautoimmune multiorgan syndrome. Int J Dermatol, 2007, 46(11), 1146–54.
[630] Helou, J; Allbritton, J; Anhalt, GJ. Accuracy of indirect immunofluorescence testing in the diagnosis of paraneoplastic pemphigus. J Am Acad Dermatol, 1995, 32(3), 441–7.
[631] Probst, C; Schlumberger, W; Stocker, W; et al. Development of ELISA for the specific determination of autoantibodies against envoplakin and periplakin in paraneoplastic pemphigus. Clin Chim Acta, 2009, 410(1–2), 13–8.
[632] Ishii, N; Hamada, T; Koga, H; Sogame, R; Ohyama, B; Fukuda, S; et al. Decline of disease activity and autoantibodiesto desmoglein 3 and envoplakin by oralprednisolone in paraneoplastic pemphigus withbenign thymoma. Eur J Dermatol, 2012, 22(4), 547–9.
[633] Bennett, DD; Busick, TL. Delayed detection of autoantibodies in paraneoplastic pemphigus. J Am Acad Dermatol, 2007, 57(6), 1094–5.
[634] Barnadas, MA; Curell, R; Alomar, A; Gelpí, C. Paraneoplastic pemphigus with negative direct immunofluorescence in epidermis or mucosa but positive findings in adnexal structures. J Cutan Pathol, 2009, 36(1), 34–8.
[635] Inaoki, M; Kaji, K; Furuse, S; et al. Pemphigus foliaceusdeveloping after metastasis of cutaneous squamouscell carcinoma to regional lymph nodes. J AmAcad Dermatol, 2001, 45, 767–70.
[636] Brandt, O; Rafei, D; Podstawa, E; et al. Differential IgG recognition of desmoglein 3 by paraneoplastic pemphigus and pemphigus vulgaris sera. J Invest Dermatol, 2012, 132(6), 1738–41.
[637] Reich, K; Brinck, U; Letschert, M; et al. Graft-versus-host disease-like immunophenotypeand apoptotic keratinocyte death in paraneoplasticpemphigus. Br J Dermatol, 1999, 141, 739–46.
[638] Lim, YJ; Chang, SE; Choi, JH; et al. Expression of inducible nitric oxide synthasein skin lesions of acute herpes zoster. J Dermatol Sci, 2002, 29(3), 201–5.
[639] Iranzo, P; Xaubet, A; Carrera, C; et al. Bronchiolitis obliterans associated withparaneoplastic pemphigus: a paraneoplastic autoimmune multiorgan syndrome. Arch Bronconeumol, 2004, 40(5), 240–3.
[640] Horn, TD; Anhalt, GJ. Histologic features of paraneoplastic pemphigus. Arch Dermatol, 1992, 128(8), 1091-5.
[641] Yong, AA; Tey, HL. Paraneoplastic pemphigus. Austral J Dermatol, 2015, 54, 241-250.
[642] Zhang, J; Qiao, QL; Chen, XX; et al. Improved outcomes after complete resection of underlying tumors for patients with paraneoplastic pemphigus: a single-center experience of 22 cases. J Cancer Res Clin Oncol, 2010, 14.
[643] Anhalt, GJ. Paraneoplastic pemphigus. Adv Dermatol, 1997, 12, 77–96, discussion 7.
[644] Hohwy, T; Bang, K; Steiniche, T; Peterslund, NA; d’Amore, F. Alemtuzumab‐induced remission of both severe paraneoplastic pemphigus and leukaemic bone marrow infiltration in a case of treatment-resistantB-cell chronic lymphocytic leukaemia. Eur J Haematol, 2004, 73(3), 206–9.
[645] Borradori, L; Lombardi, T; Samson, J; Girardet, C; Saurat, JH; Hugli, A. Anti-CD20 monoclonal antibody (rituximab) for refractory erosive stomatitis secondary toCD20+ follicular lymphoma-associated paraneoplasticpemphigus. Arch Dermatol, 2001, 137(3), 269.
[646] Heizmann, M; Itin, P; Wernli, M; Borradori, L; Bargetzi, M. Successful treatment of paraneoplastic pemphigusin follicular NHL with rituximab: report of a case andreview of treatment for paraneoplastic pemphigus inNHL and CLL. Am J Hematol, 2001, 66(2), 142–4.
[647] Barnadas, M; Roe, E; Brunet, S; et al. Therapy of paraneoplastic pemphiguswith Rituximab, a case report and review of literature. J Eur Acad Dermatol Venereol, 2006, 20(1), 69–74.
[648] Grando, S. New approaches to the treatment of pemphigus. J Invest Dermatol Symp Proc, 2004, 9, 84–91.
[649] Ekbäck, M; Uggla, B. Paraneoplastic pemphigus associated with chronic lymphocytic leukaemia: treatment with alemtuzumab. Leuk Res, 2012, 36, e190–1.
[650] Kimyai‐Asadi, A; Jih, MH. Paraneoplastic pemphigus. Int J Dermatol, 2001, 40(6), 367–72.
[651] Nousari, HC; Deterding, R; Wojtczack, H; et al. The mechanism of respiratory failure in paraneoplastic pemphigus. N Engl J Med, 1999, 340(18), 1406–10.
[652] Hashimoto, T; Ebihara, T; Dmochowski, M; et al. IgA antikeratinocyte surface autoantibodies from two types of intercellular IgA vesiculopustular dermatosis recognize distinct isoforms of desmocollin. Arch Dermatol Res, 1996, 288(8), 447–52.
[653] Hashimoto, T; Ebihara, T; Nishikawa, T. Studies of autoantigens recognized by IgA anti-keratinocyte cellsurface antibodies. J Dermatol Sci, 1996, 12(1), 10–7.
[654] Hashimoto, T; Yasumoto, S; Nagata, Y; Okamoto, T; Fujita, S. Clinical, histopathological and immunological distinction in two cases of IgA pemphigus. Clin Exp Dermatol, 2002, 27(8), 636–40.
[655] Wallach, D. Intraepidermal IgA pustulosis. J Am Acad Dermatol, 1992, 27(6 Pt 1), 993–1000.
[656] Gengoux, P; Tennstedt, D; Lachapelle, JM. Intraepidermalneutrophilic IgA dermatosis: pemphigus-like IgA deposits. Dermatology, 1992, 185(4), 311–3.
[657] Teraki, Y; Amagai, N; Hashimoto, T; Kusunoki, T; Nishikawa. T. Intercellular IgA dermatosis of childhood. Selective deposition of monomer IgA1 in the intercellular space of the epidermis. Arch Dermatol, 1991, 127(2), 221–4.
[658] Chorzelski, TP; Beutner, EH; Kowalewski, C; et al. IgA pemphigus foliaceus with a clinical presentation of pemphigus herpetiformis. J Am Acad Dermatol, 1991, 24(5 Pt 2), 839–44.
[659] Erdag, G; Qureshi, HS; Greer, KE; Patterson, JW. Immunoglobulin A pemphigus involving the perianal skin and oral mucosa: an unusual presentation. Cutis, 2007, 80(3), 218–20.
[660] Zaraa, I; Kerkeni, N; Sellami, M; Chelly, I; Zitouna, M; Makni, S; et al. IgG/IgA pemphigus with IgG and IgAantidesmoglein 3 antibodies and IgA antidesmoglein 1antibodies detected by enzyme-linked immunosorbent assay: a case report and review of the literature. Int J Dermatol, 2010, 49(3), 298–302.
[661] Kopp, T; Sitaru, C; Pieczkowski F; Schneeberger A; Fodinger D; Zillikens D; et al. (2006). IgA pemphigus—occurrence of anti-desmocollin 1 and anti-desmoglein1 antibody reactivity in an individual patient. J Dtsch Dermatol Ges, 4(12), 1045–50.
[662] Kim SC; Won JH; Chung, J; Bang, DS. IgA pemphigus: report of a case with immunoelectron localizationof bound IgA in the skin. J Am Acad Dermatol, 1996, 34(5 Pt 1), 852–4.
[663] Carayannopoulos, L; Hexham, JM; Capra, JD. Localization of the binding site for the monocyteimmunoglobulin (Ig) A-Fc receptor (CD89) to the domain boundary between C alpha2 and C alpha3 in human IgA1. J Exp Med, 1996, 183(4), 1579–86.
[664] Petropoulou, H; Politis, G; Panagakis, P; Hatziolou, E; Aroni, K; Kontochristopoulos, G. Immunoglobulin apemphigus associated with immunoglobulin A gammopathy and lung cancer. J Dermatol, 2008, 35(6), 341–5.
[665] Hodak, E; David, M; Ingber, A; Rotem, A; Hazaz, B; Shamai-Lubovitz, O; et al. The clinical and histopathological spectrum of IgA-pemphigus—report of twocases. Clin Exp Dermatol, 1990, 15(6), 433–7.
[666] Ishii, N; Ishida-Yamamoto, A; Hashimoto, T. Immunolocalization of target autoantigens in IgA pemphigus. Clin Exp Dermatol, 2004, 29(1), 62–6.
[667] Yasuda, H; Kobayashi, H; Hashimoto, T; Itoh, K; Yamane, M; Nakamura, J. Subcorneal pustular dermatosistype of IgA pemphigus, demonstration of autoantibodies to desmocollin-1 and clinical review. Br J Dermatol, 2000, 143(1), 144–8.
[668] Endo, Y; Tsujioka, K; Tanioka, M; et al. Bullous dermatosis associated with IgG antibodies specific for desmocollins. Eur J Dermatol, 2010, 20(5), 620–5.
[669] Camisa C; Warner M. Treatment of pemphigus. Dermatol Nurs, 1998, 10(2), 115–8, 23–31.
[670] McLeish, KR; Miller, FN; Stelzer, GT; Wellhausen, SR. Mechanism by which methylprednisolone inhibitsacute immune complex-induced changes in vascularperme ability. Inflammation, 1986, 10(3), 321–32.
[671] Williams, RN; Paterson, CA. The influence of topicalcorticosteroid therapy upon polymorphonuclear leukocytedistribution, vascular integrity and ascorbate levels in endotoxin-induced inflammation of the rabbit eye. Exp Eye Res, 1987, 44(2), 191–8.
[672] Zurier, RB; Weissman, G. Anti-immunologic and antiinflammatory effects of steroid therapy. Med Clin N Am, 1973, 57(5), 1295–307.
[673] Gruss, C; Zillikens, D; Hashimoto, T; et al. Rapid response of IgA pemphigus of subcorneal pustular dermatosis type to treatment with isotretinoin. J Am Acad Dermatol, 2000, 43(5 Pt2), 923–6.
[674] Ruiz-Genao, DP; Hernandez-Nunez, A; Hashimoto, T; Amagai, M; Fernandez-Herrera J; Garcia-Diez, A. A case of IgA pemphigus successfully treated withacitretin. Br J Dermatol, 2002, 147(5), 1040–2.
[675] Howell, SM; Bessinger, GT; Altman, CE; Belnap, CM. Rapid response of IgA pemphigus of the subcornealpustular dermatosis subtype to treatment with adalimumab and mycophenolate mofetil. J Am Acad Dermatol, 2005, 53(3), 541–3.
[676] Mahalingam, M. Follicular acantholysis: a subtle clue to the early diagnosis of pemphigus vulgaris. Am J Dermatopathol, 2005, 27, 237–9.
[677] Emmerson, RW; Wilson, JE. Eosinophilic spongiosis in pemphigus. Arch Dermatol, 1968, 97, 252–7.
[678] Ahmed, AR; Blose, DA. Pemphigus vegetans. Neumann type and Hallopeau type. Int J Dermatol, 1984, 23, 135–41.
[679] Sladden, C; Kirchhof, MG; Crawford, RI. Biopsylocation for direct immunofluorescence in patients with suspected bullous pemphigoid impacts probability of a positive test result. J Cutan Med Surg, 2014, 18, 392–6.
[680] Jablonska, S; Chorzelski, T; Beutner, EH; et al. Herpetiform pemphigus: a variable pattern of pemphigus. Int J Dermatol, 1975, 14, 353–9.
[681] Kanitakis, J; Wang, YZ; Roche, P; et al. Immuno histopathological study of autoimmune pemphigus. Lack of strictly specific histological and indirect immunofluorescence criteria for paraneoplastic pemphigus. Dermatology, 1994, 188, 282–5.
[682] Wang, J; Kwon, J; Ding, X; Fairley, JA; Woodley, DT; Chan, LS. Nonsecretory IgA1 autoantibodies targeting desmosomal component desmoglein 3 inintraepidermal neutrophilic IgA dermatosis. Am J Pathol, 1997, 150, 1901–7.
[683] Borradori, L; Saada, V; Rybojad, M; et al. Oral intraepidermalIgA pustulosis and Crohn’s disease. Br J Dermatol, 1992, 126, 383–6.
[684] Storch, WB. Ed. Immunofluorescence in Clinical Immunology. Germany, 2000, Pp. 231. ISBN. 978-3-7643-6182-2.
[685] Ullman, S. Immunofluorescence and diseases of the skin. Acta Derm Venereol Suppl (Stockh), 1988, 140, 1–31.
[686] Michel, B; Milner, Y; David, K. Preservation of tissue-fixed immunoglobulins in skin biopsies of patients with lupus erythematosus and bullous diseases-preliminary report. J Invest Dermatol, 1973, 59, 449–52.
[687] Vaughan Jones, SA; Salas, J; McGrath, JA; Palmer, I; Bhogal, GS; Black, MM. A retrospective analysis of tissue-fixed immunoreactants from skin biopsiesmaintained in Michel’s medium. Dermatology, 1994, 189 Suppl 1, 131–2.
[688] Vodegel, RM; de Jong, MC; Meijer, HJ; Weytingh, MB; Pas, HH; Jonkman, MF. Enhanced diagnostic immunofluorescence using biopsies transported insaline. BMC Dermatol, 2004, 4, 10.
[689] Arbesman, J; Grover, R; Helm, TN; Beutner, EH. Can direct immunofluorescence testing still be accurate if performed on biopsy specimens after brief in advertent immersion in formalin? J Am Acad Dermatol, 2011, 65, 106–11.
[690] Beutner, EH; Lever, WF; Witebsky, E; Jordon, R; Chertock, B. Autoantibodies in pemphigus vulgaris, response to an intercellular substance of epidermis. JAMA, 1965, 192, 682–8.
[691] Ratnam, KV; Pang, BK. Pemphigus in remission: value of negative direct immunofluorescence in management. J Am Acad Dermatol, 1994, 30, 547–50.
[692] de Messias, IT; von Kuster, LC; Santamaria, J; Kajdacsy-Balla, A. Complement and antibody depositionin Brazilian pemphigus foliaceus and correlationof disease activity with circulating antibodies. Arch Dermatol, 1988, 124, 1664–8.
[693] Nikolskaia, OV; Nousari, CH; Anhalt, GJ. Paraneoplasticpemphigus in association with Castleman’s disease. Br J Dermatol, 2003, 149, 1143–51.
[694] Zhou, S; Wakelin, SH; Allen, J; Wojnarowska, F. Blister fluid for the diagnosis of subepidermal immunobullousdiseases: a comparative study of basement membrane zone autoantibodies detected in blister fluid and serum. Br J Dermatol, 1998, 139, 27–32.
[695] Allen, J; Shears, E; Powell, J; Wojnarowska, F. Assessment of skin basement membrane zone antibodiesin the urine of patients with acquired subepidermalimmunobullous diseases. Br J Dermatol, 2001, 144, 540–5.
[696] Judd, KP; Lever, WF. Correlation of antibodies in skin and serum with disease severity in pemphigus. ArchDermatol, 1979, 115, 428–32.
[697] Ahmed, AR; Workman, S. Presence in serum samples of 14 patients without pemphigus. Arch Dermatol, 1983, 119, 17–21.
[698] Creswell, SN; Black, MM; Bhogal, B; Skeete, MV. Correlation of circulating intercellular antibodytitres in pemphigus with disease activity. Clin ExpDermatol, 1981, 6, 477–83.
[699] Feibelman, C; Stolzner, G; Provost, TT. Pemphigusvulgaris. Superior sensitivity of monkey esophagusin the determination of pemphigus antibody. Arch Dermatol, 1981, 117, 561–2.
[700] Matis, WL; Anhalt, GJ; Diaz, LA; Rivitti, EA; Martins, CR; Berger, RS. Calcium enhances the sensitivity of immunofluorescence for pemphigus antibodies. J Invest Dermatol, 1987, 89, 302–4.
[701] Squiquera, HL; Diaz, LA; Sampaio, SA; et al. Serologic abnormalitiesin patients with endemic pemphigus foliaceus (Fogoselvagem), their relatives, and normal donors fromendemic and non-endemic areas of Brazil. J Invest Dermatol, 1988, 91, 189–91.
[702] Rowilson-Cunha, P; Bystryn, JC. Sensitivity of indirect immunofluorescence and immunoblotting for the detection of intercellular antibodies inendemic pemphigus foliaceus (fogo selvagem). Int J Dermatol, 1999, 38, 41–5.
[703] Jiao, D; Bystryn, JC. Sensitivity of indirect immunofluorescence, substrate specificity, and immunoblottingin the diagnosis of pemphigus. J Am Acad Dermatol, 1997, 37, 211–6.
[704] Su, WP; Oursler, JR; Muller, SA. Paraneoplastic pemphigus: a case with high titer of circulating antibasement membrane zone autoantibodies. J Am Acad Dermatol, 1994, 30, 841–4.
[705] Liu, AY; Valenzuela, R; Helm, TN; Camisa, C; Melton, AL; Bergfeld, WF. Indirect immunofluorescence onrat bladder transitional epithelium: a test with highspecificity for paraneoplastic pemphigus. J Am Acad Dermatol, 1993, 28, 696–9.
[706] Foedinger, D; Sterniczky, B; Elbe, A; Anhalt, G; Wolff, K; Rappersberger, K. Autoantibodies against desmoplakin I and II define a subset of patients witherythema multiforme major. J Invest Dermatol, 1996, 106, 1012–6.
[707] Mimouni, D; Foedinger, D; Kouba, DJ; Orlow, SJ; Rappersberger, K; Sciubba, JJ; et al. Mucosal dominant pemphigus vulgaris with anti-desmoplakinautoantibodies. J Am Acad Dermatol, 2004, 51, 62–7.
[708] Lleo, A; Invernizzi, P; Gao, B; Podda, M; Gershwin, ME. Definition of human autoimmunity—autoantibodies versus autoimmune disease. Autoimmun Rev, 2010, 9(5), A259–66.
[709] Cunha, PR; Barraviera, SR. Autoimmune bullous dermatoses. An Bras Dermatol, 2009, 84(2), 111–24.
[710] Vaughan, FL; Bernstein, IA. Molecular aspects ofcontrol in epidermal differentiation. Mol Cell Biochem, 1976, 12(3), 171–9.
[711] Brooke, MA; Nitoiu, D; Kelsell, DP. Cell-cell connectivity: desmosomes and disease. J Pathol, 2012, 226(2), 158–71.
[712] Green, KJ; Simpson, CL. Desmosomes: new perspectiveson a classic. J Invest Dermatol, 2007, 127(11), 2499–515.
[713] Sterk, LM; Geuijen, CA; Oomen, LC; Calafat, J; Janssen, H; Sonnenberg, A. The tetraspan molecule CD151, a novel constituent of hemidesmosomes, associates with the integr in alpha6 beta4 and may regulate the spatial organization of hemidesmosomes. J Cell Biol, 2000, 149(4), 969–82.
[714] Tsuruta, D; Kobayashi, H; Imanishi, H; Sugawara, K; Ishii, M; Jones, JC. Laminin-332-integrin interaction, atarget for cancer therapy? Curr Med Chem, 2008, 15(20), 1968–75.
[715] Koster, J; Geerts, D; Favre, B; Borradori, L; Sonnenberg, A. Analysis of the interactions between BP180, BP230, plectin and the integrin alpha6beta4 importantfor hemidesmosome assembly. J Cell Sci, 2003, 116(Pt2), 387–99.
[716] Koster, J; van Wilpe, S; Kuikman, I; Litjens, SH; Sonnenberg, A. Role of binding of plectin to the integrinbeta4 subunit in the assembly of hemidesmosomes. Mol Biol Cell, 2004, 15(3), 1211–23.
[717] Schmidt, E; Brocker, EB; Zillikens, D. Pemphigus. Loss of desmosomal cell-cell contact. Hautarzt, 2000, 51(5), 309–18.
[718] Fontao, L; Favre, B; Riou, S; et al. Interaction of the bullous pemphigoid antigen 1 (BP230) and desmoplakin with intermediate filaments is mediated by distinct sequences within their COOH terminus. Mol Biol Cell, 2003, 14(5), 1978–92.
[719] Karashima, T; Tsuruta, D; Hamada, T; et al. Interaction of plectin andintermediate filaments. J Dermatol Sci, 2012, 66(1), 44–50.
[720] Monshi, B; Marker, M; Feichtinger, H; et al. Pemphigus vegetans— immunopathological findings in a rare variant of pemphigus vulgaris. J Dtsch Dermatol Ges, 2010, 8(3), 179–83.
[721] Tsuruta, D; Kobayashi H. Recent patents in pemphigus research, prophylaxis, diagnosis and treatment in USA (1988–2006). Recent Pat Inflamm Allergy Drug Discov, 2007, 1(1), 77–81.
[722] Tateishi, C; Tsuruta, D; Nakanishi, T; et al. Antidesmocollin-1 antibody- positive, antidesmoglein antibody-negativepemphigus herpetiformis. J Am Acad Dermatol, 2010, 63(1), e8–10.
[723] Harman, KE. New laboratory techniques for theassessment of acquired immunobullous disorders. Clin Exp Dermatol, 2002, 27(1), 40–6.
[724] Ishii, K; Amagai, M; Hall, RP; et al. Characterization of autoantibodies in pemphigus using antigen-specific enzyme-linkedimmunosorbent assays with baculovirus-expressed recombinant desmogleins. J Immunol, 1997, 159(4), 2010–7.
[725] Miida, H; Fujiwara, H; Ito, M. Association betweeneffective dose of prednisolone, alone or in conjunctionwith other immunosuppressants, and titre ofanti-bullous pemphigoid 180 antibody: a retrospectivestudy of 42 cases. Clin Exp Dermatol, 2011, 36(5), 485–8.
[726] Lee, JB; Fumimori, T; Kurose, K; Mori, O; Hashimoto, T. A case of bullous pemphigoid successfully treated byplasmapheresis: assessment of the change in titers ofcirculating antibodies by immunoblotting and enzyme-linked immunosorbent assay. J Dermatol, 2003, 30(4), 326–31.
[727] Natsuga, K; Nishie, W; Shinkuma, S; et al. Circulating IgA and IgE autoantibodies in antilaminin-332 mucous membrane pemphigoid. Br J Dermatol, 2010, 162(3), 513–7.
[728] Dmochowski, M; Hashimoto, T; Bhogal, BS; Black, MM; Zone, JJ; Nishikawa, T. Immunoblotting studiesof linear IgA disease. J Dermatol Sci, 1993, 6(3), 194–200.
[729] Ohata, Y; Hashimoto, T; Nishikawa, T. Comparativestudy of autoantigens for various bullous skin diseasesby immunoblotting using different dermo-epidermal separation techniques. Clin Exp Dermatol, 1995, 20(6), 454–8.
[730] Kowalczyk, AP; Anderson, JE; Borgwardt, JE; Hashimoto, T; Stanley, JR; Green, KJ. Pemphigus sera recognize conformationally sensitive epitopes in theamino-terminal region of desmoglein-1. J Invest Dermatol, 1995, 105(2), 147–52.
[731] Nagata, Y; Karashima, T; Watt, FM; Salmhofer, W; Kanzaki, T; Hashimoto, T. Paraneoplastic pemphigussera react strongly with multiple epitopes on the various regions of envoplakin and periplakin, except for the c-terminal homologous domain of periplakin. J Invest Dermatol, 2001, 116(4), 556–63.
[732] Prost, C; Dubertret, L; Fosse, M; Wechsler, J; Touraine, R. A routine immuno-electron microscopic technique for localizing an auto-antibody on epidermal basementmembrane. Br J Dermatol, 1984, 110(1), 1–7.
[733] Prost, C; Labeille, B; Chaussade, V; Guillaume, JC; Martin, N; Dubertret, L. Immunoelectron microscopyin subepidermal autoimmune bullous diseases: a prospectivestudy of IgG and C3 bound in vivo in 32 patients. J Invest Dermatol, 1987, 89(6), 567–73.
[734] Bédane, C; Prost, C; Bernard, P; Catanzano, G; Bonnetblanc, JM; Dubertret, L. Cicatricial pemphigoidantigen differs from bullous pemphigoid antigen byits exclusive extracellular localization: a study byindirect immunoelectronmicroscopy. J Invest Dermatol, 1991, 97(1), 3–9.
[735] Bédane, C; McMillan, JR; Balding, SD; et al. Bullous pemphigoid and cicatricial pemphigoidautoantibodies react with ultrastructurally separable epitopes on the BP180 ectodomain: evidence that BP180 spans the lamina lucida. J Invest Dermatol, 1997, 108(6), 901–7.
[736] Tanaka, H; Ishida-Yamamoto, A; Hashimoto, T; et al. A novel variant ofacquired epidermolysis bullosa with autoantibodies against the central triple-helical domain of type VII collagen. Lab Invest, 1997, 77(6), 623–32.
[737] Ishiko, A; Shimizu, H; Masunaga, T; et al. 97-kDa linear IgA bullous dermatosis(LAD)antigen localizes to the lamina lucida ofthe epidermal basement membrane. J Invest Dermatol, 1996, 106(4), 739–43.
[738] Tidman, MJ; Eady, RA. Ultrastructural morphometry of normal human dermal-epidermal junction. The influence of age, sex, and body region on laminar and nonlaminar components. J Invest Dermatol, 1984, 83(6), 448–53.
[739] Liu, Z; Li, N; Diaz, LA. Immunopathological mechanismsof acantholysis in pemphigus vulgaris: an explanation by ultrastructural observations. J Invest Dermatol, 2004, 122(5), XIII–XIV.
[740] Shimizu, H; Masunaga, T; Ishiko, A; Kikuchi, A; Hashimoto, T; Nishikawa, T. Pemphigus vulgaris and pemphigus foliaceus sera show an inversely graded binding pattern to extracellular regions of desmosomesin different layers of human epidermis. J Invest Dermatol, 1995, 105(2), 153–9.
[741] Zhou, S; Ferguson, DJ; Allen, J; Wojnarowska, F. The location of binding sites of pemphigus vulgaris and pemphigus foliaceus autoantibodies: a postembedding immunoelectron microscopic study. Br J Dermatol, 1997, 136(6), 878–83.
[742] Akiyama, M; Hashimoto, T; Sugiura, M; Nishikawa, T. Ultrastructural localization of pemphigus vulgarisand pemphigus foliaceus antigens in cultured humans quamous carcinoma cells. Br J Dermatol, 1991, 125(3), 233–7.
[743] Kárpáti, S; Amagai, M; Prussick, R; Cehrs, K; Stanley, JR. Pemphigus vulgaris antigen, a desmoglein type of cadherin, is localized within keratinocyte desmosomes. J Cell Biol, 1993, 122(2), 409–15.
[744] Chorzelski, T; Biczysko, W; Dabrowski, J; Jarzabek, M. Ultrastructural localization of pemphigus autoantibodies. J Invest Dermatol, 1968, 50(1), 36–40.
[745] Wolff, K; Schreiner, E. Ultrastructural localization of pemphigus autoantibodies within the epidermis. Nature, 1971, 229(5279), 59–61.
[746] Hönigsmann, H; Holubar, K; Wolff, K; Beutner, EH. Immunochemical localization of in vivo boundimmunoglobulins in pemphigus vulgaris epidermis. Employment of a peroxidase-antiperoxidase multisteptechnique for light and electron microscopy. Arch Dermatol Res, 1975, 254(2), 113–20.
[747] Patel, HP; Diaz, LA; Anhalt, GJ; Labib, RS; Takahashi, Y. Demonstration of pemphigus antibodies on the cell surface of murine epidermal cell monolayersand their internalization. J Invest Dermatol, 1984, 83(6), 409–15.
[748] Wang, W; Amagai, M; Ishiko, A. Desmosome splitting is a primary ultrastructural change in the acantholysis of pemphigus. J Dermatol Sci, 2009, 54(1), 59–61.
[749] Diercks, GF; Pas, HH; Jonkman, MF. The ultrastructure of acantholysis in pemphigus vulgaris. Br JDermatol, 2009, 160(2), 460–1.
[750] Wilgram, G; Caulfield, J; Lever, W. An electronmicroscopic study of acantholysis in pemphigus vulgaris. J Invest Dermatol, 1961, 36(5), 373–82.
[751] Wilgram, GF; Caulfield, JB; Madgic, EB. An electronmicroscopic study of acantholysis and dyskeratos is in pemphigus foliaceus: with a special note on peculiarintracytoplasmic bodies. J Invest Dermatol, 1964, 43, 287–99.
[752] Hashimoto, K; Lever, WF. An electron microscopicstudy on pemphigus vulgaris of the mouth and the skin with special reference to the intercellularcement. J Invest Dermatol, 1967, 48(6), 540–52.
[753] Sotto, MN; Shimizu, SH; Costa, JM; De Brito, T. South American pemphigus foliaceus: electron microscopy and immunoelectron localization of boundimmunoglobulin in the skin and oral mucosa. Br J Dermatol, 1980, 102(5), 521–7.
[754] Hu, CH; Michel, B; Schiltz, JR. Epidermal acantholysisinduced in vitro by pemphigus autoantibody. An ultrastructural study. Am J Pathol, 1978, 90(2), 345–62.
[755] Barnett, ML; Beutner, EH; Chorzelski, TP. Organculture studies of pemphigus antibodies. II. Ultrastructural comparison between acantholytic changes in vitro and human pemphigus lesions. J Invest Dermatol, 1977, 68(5), 265–71.
[756] Lanza, A; De Rosa, A; Femiano, F; et al. Internalization of non-clustered desmoglein 1 withoutdepletion of desmoglein 1 from adhesion complexesin an experimental model of the autoimmunedisease pemphigus foliaceus. Int J Immunopathol Pharmacol, 2007, 20(2), 355–61.
[757] Oktarina, DA; van der Wier, G; Diercks, GF; Jonkman, MF; Pas, HH. IgG-induced clustering ofdesmogleins 1 and 3 in skin of patients withpemphigus fits with the desmoglein nonassemblydepletion hypothesis. Br J Dermatol, 2011, 165(3), 552–62.
[758] Costello, MJ; Jaimovich, L; Dannenberg, M. Treatment of pemphigus with corticosteroids; study of fifty-two patients. J Am Med Assoc, 1957, 165(10), 1249–55.
[759] Almugairen, N. Assessment of the rate of long term complete remission off therapy in patients with pemphigus treated with different regimens including medium- and high-dose corticosteroids. J Am Acad Dermatol, 2013, 069(4), 583–8.
[760] Dick, SE; Werth, VP. Pemphigus: a treatment update. Autoimmunity, 2006, 39(7), 591–9.
[761] Mimouni, D; Nousari, CH; Cummins, DL; et al. Differences and similarities among expert opinions on the diagnosis and treatment of pemphigus vulgaris. J Am Acad Dermatol, 2003, 49, 1059–1062.
[762] Sagi, L. The role of the rapeutic plasma exchangein pemphigus vulgaris. J Eur Acad Dermatol Venereol, 2011, 25(1), 82–6.
[763] Fernandes, NC; Perez, M. Treatment of pemphigusvulgaris and pemphigus foliaceus: experience with 71 patients over a 20 year period. Rev Inst Med Trop Sao Paulo, 2001, 43(1), 33–6.
[764] Ratnam, KV; Phay, KL; Tan, CK. Pemphigus therapy with oral prednisolone regimens. A 5-year study. Int J Dermatol, 1990, 29(5), 363–7.
[765] Hofmann, SC. Results of a survey of Germandermatologists on the therapeutic approaches to pemphigusand bullous pemphigoid. J Dtsch Dermatol Ges, 2009, 7(3), 227–33.
[766] Schmidt, E. Rituximab in autoimmune bullousdiseases: mixed responses and adverse effects. Br J Dermatol, 2007, 156(2), 352–6.
[767] Kasperkiewicz, M; Schmidt, E; Zillikens, D. Current therapy of the pemphigus group. Clin Dermatol., 2012, 30(1), 84–94.
[768] Dehen, L. Comparative study of the developmentand prognosis of pemphigus vulgaris and seborrheicpemphigus. Ann Dermatol Venereol, 1993, 120(12), 874–8.
[769] Lever, WF; Schaumburg-Lever, G. Treatment of pemphigus vulgaris. Results obtained in 84 patients between 1961 and 1982. Arch Dermatol, 1984, 120(1), 44–7.
[770] Lapidoth, M. The efficacy of combined treatment with prednisone and cyclosporine in patients with pemphigus: preliminary study. J Am Acad Dermatol, 1994, 30(5 Pt 1), 752–7.
[771] Lever, WF; White, H. Treatment of pemphigus with corticosteroids. Results obtained in 46 patients over aperiod of 11 years. Arch Dermatol, 1963, 87, 12–26.
[772] Hashimoto, T. Treatment strategies for pemphigus vulgaris in Japan. Expert Opin Pharmacother, 2008, 9(9), 1519–30.
[773] Toth, GG; van de Meer, JB; Jonkman, MF. Dexamethasone pulse therapy in pemphigus. J Eur Acad Dermatol Venereol, 2002, 16(6), 607–11.
[774] Mentink, LF; Mackenzie, MW; Toth, GG; et al. Randomized controlled trial of adjuvant oral dexamethasone pulse therapy in pemphigus vulgaris: PEMPULS trial. Arch Dermatol, 2006, 142, 570–576.
[775] Aberer, W. Azathioprine in the treatment of pemphigusvulgaris. A long-term follow-up. J Am Acad Dermatol, 1987, 16(3 Pt 1), 527–33.
[776] Benoit Corven C. Treatment of pemphigus vulgarisby azathioprine and low doses of prednisone (Lever scheme). Ann Dermatol Venereol, 2003, 130(1Pt 1), 13–5.
[777] Mourellou, O. The treatment of pemphigusvulgaris. Experience with 48 patients seen over an11-year period. Br J Dermatol, 1995, 133(1), 83–7.
[778] Akhtar, SJ; Hasan, MU. Treatment of pemphigus: a local experience. J Pak Med Assoc, 1998, 48(10), 300–4.
[779] Chaidemenos, G. High dose oral prednisonevs. prednisone plus azathioprine for the treatment of oral pemphigus: a retrospective, bi-centre, comparativestudy. J Eur Acad Dermatol Venereol, 2011, 25(2), 206–10.
[780] Sebaratnam, D; Murrell, DF. Treatment of pemphigusvulgaris and pemphigus foliaceus. Expert Rev Dermatol, 2009, 4(5), 469–81.
[781] Martin, LK; Werth, VP; Villaneuva, EV; Murrell, DF. Asystematic review of randomized controlled trials forpemphigus vulgaris and pemphigus foliaceus. J Am Acad Dermatol, 2011, 64(5), 903–8.
[782] Anstey, A; Wakelin, S; Reynolds, N. Guidelines for prescribingazathioprine in dermatology. Br J Dermatol, 2004, 151(6), 1123–32.
[783] Pasricha, J; Sood, V; Minocha, Y. Treatment of pemphiguswith cyclophosphamide. Br J Dermatol, 1975, 93(5), 573–6.
[784] Chams-Davatchi, C; Esmaili, N; Daneshpazhooh, M; et al. Randomized controlled open-label trial of four treatment regimens for pemphigus vulgaris. J Am Acad Dermatol, 2007, 57, 622–8.
[785] Rose, E; Wever, S; Zilliken, D; et al. Intravenousdexamethasone- cyclophosphamide pulse therapy in comparison with oral methylprednisolone- azathioprinetherapy in patients with pemphigus vulgaris: results of amulticenter prospectively randomized study. J Dermatol Ges, 2005, 3 (3), 200–6.
[786] Powell, AM; Albert, S; Al Fares, S; Harman, KE; Setterfield, J; Bhogal, B; Black MM. An evaluation of the usefulness of mycophenolate mofetil in pemphigus. Br J Dermatol, 2003, 149, 138–45.
[787] Qin, Y; Zhang, F; Shen, B; Liu, Y; Qiu, J; Guo, Y; Fan, Y. Efficacy and safety of enteric-coated mycophenolate sodium in patients with de novo and maintenance renal transplantation. Int J Clin Pract Suppl, 2014, 181, 17-22.
[788] Zwerner, J; Fiorentino, D. Mycophenolate mofetil. Dermatol Ther, 2007, 20(4), 229–38.
[789] Nousari, H; Anhalt, G. Pemphigus and bullous pemphigoid. Lancet, 1999, 354, 667–72.
[790] Orvis, AK; Wesson, SK; Breza, Jr TS; Church, AA; Mitchell, CL; Watkins, SW. Mycophenolate mofetil indermatology. J Am Acad Dermatol, 2009, 60, 183–99, quiz 200–182.
[791] Mimouni, D. Treatment of pemphigus vulgaris and pemphigus foliaceus with mycophenolatemofetil. Arch Dermatol, 2003, 139(6), 739.
[792] Scheinfeld, N. Red blood cell anemia in a patient withpemphigus vulgaris induced by the use of mycophenolatemofetil and prednisone. J Dermatol Treat, 2007, 18(4), 243–5.
[793] Sterneck, M. Mycophenolate mofetil for preventionof liver allograft rejection: initial results of a controlled clinical trial. Ann Transplant, 2000, 5(1), 43–6.
[794] Lever, WF; Schaumburg-Lever, G. Immunosuppressantsand prednisone in pemphigus vulgaris: the rapeutic results obtained in 63 patients between 1961 and 1975. Arch Dermatol, 1977, 113(9), 1236–41.
[795] Lever, WF. Methotrexate and prednisone in pemphigusvulgaris: the rapeutic results obtained in 36 patients between 1961 and 1970. Arch Dermatol, 1972, 106(4), 491.
[796] Mashkilleyson, N; Mashkilleyson, A. Mucous membranemanifestations of pemphigus vulgaris. A25-year survey of 185 patients treated with corticosteroidsor with combination of corticosteroids with methotrexate or heparin. Acta Derm Venereol, 1988, 68(5), 413.
[797] Smith, TJ; Bystryn, JC. Methotrexate as an adjuvanttreatment for pemphigus vulgaris. Arch Dermatol, 1999, 135(10), 1275.
[798] Gürcan, H; Razzaque Ahmed, A. Analysis of currentdata on the use of methotrexate in the treatment of pemphigus and pemphigoid. Br J Dermatol, 2009, 161(4), 723–31.
[799] Chrysomallis, F. Treatment of oral pemphigusvulgaris. Int J Dermatol, 1994, 33(11), 803–7.
[800] Ioannides, D; Chrysomallis, F; Bystryn, JC. Ineffectiveness of cyclosporine as an adjuvant to corticosteroids in the treatment of pemphigus. Arch Dermatol, 2000, 136(7), 868.
[801] Bystryn, JC; Steinman, NM. The adjuvant therapy of pemphigus. An update. Arch Dermatol, 1996, 132(2), 203–12.
[802] Werth, VP; Fivenson, D; Pandya, AG; et al. Multicenter randomized, double blind, placebo-controlled, clinical trial of dapsone as a glucocorticoid-sparing agent in the maintenance-phase pemphigus vulgaris. ArchDermatol, 2008, 144(1), 25–32.
[803] Gurcan, HM; Ahmed, AR. Efficacy of dapsone in thetreatment of pemphigus and pemphigoid: analysis of current data. Am J Clin Dermatol, 2009, 10(6), 383–96.
[804] Calebotta, A. Pemphigus vulgaris: benefits of tetracycline as adjuvant therapy in a series of thirteen patients. Int J Dermatol, 1999, 38(3), 217–21.
[805] Alpsoy, E. Is the combination of tetracycline and nicotinamide therapy alone effective in pemphigus? Arch Dermatol, 1995, 131(11), 1339.
[806] Chaffins, ML; Collison, D; Fivenson, DP. Treatment of pemphigus and linear IgA dermatosis with nicotinamideand tetracycline: a review of 13 cases. J Am Acad Dermatol, 1993, 28(6), 998.
[807] Turner, MS; Sutton, D; Sauder, DN. The use of plasmapheresis and immunosuppression in the treatment of pemphigus vulgaris. J Am Acad Dermatol, 2000, 43(6), 1058–64.
[808] Roujeau, JC. Plasma exchange in pemphigus. Uncontrolled study of ten patients. Arch Dermatol, 1983, 119(3), 215–21.
[809] Tan-Lim, R; Bystryn, JC. Effect of plasmapheresis therapy on circulating levels of pemphigus antibodies. J Am Acad Dermatol, 1990, 22(1), 35–40.
[810] Guillaume, JC. Controlled study of plasma exchange in pemphigus. Arch Dermatol, 1988, 124(11), 1659–63.
[811] Braun, N; Kadar, JG; Risler, T. Therapeutic immunoadsorption—its role in clinical practice. Transfus Sci, 1998, 19(Suppl), 65–9.
[812] Eming, R; Hertl, M. Immunoadsorption in pemphigus. Autoimmunity, 2006, 39(7), 609–16.
[813] Schoen, H. Immunoapheresis in paraneoplasticpemphigus. Arch Dermatol, 1998, 134(6), 706–10.
[814] Luftl, M. Successful removal of pathogenic autoantibodiesin pemphigus by immunoadsorption with a tryptophan-linked polyvinylalcohol adsorber. Br J Dermatol, 2003, 149(3), 598–605.
[815] Frost, N. Treatment of pemphigus vulgaris with protein A immunoadsorption, case report of long- termhistory showing favorable outcome. Ann N Y Acad Sci, 2005, 1051, 591–6.
[816] Schneider, KM. Plasmapheresis and immunoadsorption: different techniques and their current role inmedical therapy. Kidney Int Suppl, 1998, 64, S61–5.
[817] Amagai, M; Ikeda, S; Shimizu, H; et al. A randomized double-blind trial of intravenousimmunoglobulin for pemphigus. J Am Acad Dermatol, 2009, 60(4), 595–603.
[818] Prins, C; Gelfand, EW; French, LE. Intravenousimmunoglobulin: properties, mode of action andpractical use in dermatology. Acta Derm Venereol, 2007, 87(3), 206–18.
[819] Zhu, KY. Intravenous immunoglobulin suppresses experimental myasthenia gravis: immunological mechanisms. J Neuroimmunol, 2006, 176(1–2), 187–97.
[820] Aoyama, Y. What’s new in i.v. immunoglobulin therapyand pemphigus: high-dose i.v. immunoglobulintherapy and its mode of action for treatment of pemphigus. J Dermatol, 2010, 37(3), 239–45.
[821] Green, MG; Bystryn, JC. Effect of intravenousimmunoglobulin therapy on serum levels of IgG1and IgG4 antidesmoglein 1 and antidesmoglein 3 antibodies in pemphigus vulgaris. Arch Dermatol, 2008, 144(12), 1621–4.
[822] Mimouni, D. Protective effect of intravenous immunoglobulin (IVIG) in an experimental model of pemphigusvulgaris. Clin Exp Immunol, 2005, 142(3), 426–32.
[823] Bystryn, J; Jiao, D; Natow, S. Treatment of pemphiguswith intravenous immunoglobulin. J Am Acad Dermatol, 2002, 47(3), 358–63.
[824] Arnold, D; Burton, J; Shine, B; Wojnarowska, F; Misbah, S. An ‘n-of-1’ placebo-controlled crossover trial ofintravenous immunoglobulin as adjuvant therapy. Br J Dermatol, 2009, 160(5), 1098-102.
[825] Di Gaetano, N. Complement activation determines the therapeutic activity of rituximab in vivo. J Immunol, 2003, 171(3), 1581–7.
[826] Looney, RJ. B cells as a therapeutic target in autoimmune diseases other than rheumatoid arthritis. Rheumatology (Oxford), 2005, 44 Suppl 2, ii13–7.
[827] Zambruno, G; Borradori, L. Rituximab immunotherapy in pemphigus: therapeutic effects beyond B-cell depletion. J Invest Dermatol, 2008, 128(12), 2745–7.
[828] Herrmann, G; Hunzelmann, N; Engert, A. Treatment ofpemphigus vulgaris with anti-CD20 monoclonal antibody (rituximab). Br J Dermatol, 2003, 148(3), 602–3.
[829] Faurschou, A; Gniadecki, R. Two courses of rituximab (anti-CD20 monoclonal antibody) for recalcitrant pemphigus vulgaris. Int J Dermatol, 2008, 47(3), 292–4.
[830] Hertl, M. Recommendations for the use of rituximab (anti-CD20 antibody) in the treatment of autoimmunebullous skin diseases. J Dtsch Dermatol Ges, 2008, 6(5), 366–73.
[831] Dupuy, A. Treatment of refractory pemphigus vulgaris with rituximab (anti-CD20 monoclonal antibody). Arch Dermatol, 2004, 140(1), 91–6.
[832] Morrison, LH. Therapy of refractory pemphigus vulgaris with monoclonal anti-CD20 antibody (rituximab). J Am Acad Dermatol, 2004, 51(5), 817–9.
[833] Bikowski, J; Pillai, R. The position not the presence of the halogen in corticosteroids infl uences potency andside effects. Drugs Dermatol, 2006, 5(2), 125–30.
[834] Williams, LC; Nesbitt, Jr LT. Update on systemic glucocorticosteroids in dermatology. Dermatol Clin, 2001, 19(1), 63–77.
[835] McClain, R; Yentzer, B; Fledman, S. Comparison of skin concentration following topical versus oral corticosteroid treatment: reconsidering the treatment of common inflammatory dermatoses. Drugs Dermatol, 2009, 8(12), 1076–9.
[836] Murrell, D; Daniel, B; Joly, P; et al. Definitions and outcome measures for bullous pemphigoid: recommendations by an international panel of experts. J Am Acad Dermatol, 2012, 66(3), 479–85.
[837] Martin, L; Agero, AL; Werth, V; et al. Interventions for Pemphigus Vulgaris and Pemphigus Foliaceus (Review). Cochrane Database Syst Rev, 2009, (1), CD006263.
[838] Harman, KE; Albert, S; Black, MM. Guidelines for the management of pemphigus vulgaris. Br J Dermatol, 2003, 149, 926–37.
[839] Lapiere, K; Caers, S; Lambert, J. A case of long standing pemphigus vulgaris on the scalp. Dermatology, 2004, 209, 162–3.
[840] Baykal, C; Azizlerli, G; Thoma-Uszynski, S; et al. Pemphigus vulgaris localized to the nose and cheeks. J Am Acad Dermatol, 2002, 47, 875–8.
[841] Dagistan, S; Goregen, M; Miloglu, O; et al. Oral pemphigus vulgaris: a case report with review of the literature. J Oral Sci, 2008, 50(3), 359–62.
[842] Hanna, A; Sebaratnam, D; Chee, S; et al. The development of a disease-specific quality of lifeinstrument for autoimmune bullous dermatoses: the ABQOL. J Invest Dermatol, 2011, 131 Suppl 2, S33.
[843] Gulko, PS; Mulloy, AL. Glucocorticoid-induced osteoporosis: pathogenesis, prevention and treatment. Clin Exp Rheumatol, 1996, 14, 199–206.
[844] Compston, J. Management of glucocorticoid-induced osteoporosis. Nat Rev Rheumatol, 2010, 6, 82–8.
[845] Stoch, SA; Saag, KG; Greenwald, M; et al. Onceweeklyoral alendronate 70mg in patients with glucocorticoidinduced bone loss: a 12 month randomizes, placebo controlled clinical trial. J Rheumatol, 2009, 36(8), 1705–14.
[846] Cohen, S; Levy, R; Keller, M; et al. Risendronate therapyprevents corticosteroid induced bone loss: atwelve month, multicenter, randomized, double blindplacebo controlled parallel group study. Arthritis Rheumatol, 1999, 42(11), 2309–18.
[847] Minden, S; Orav, J; Schildkraut, J. Hypomanic reactionsto ACTH and prednisone in treatment for multiplesclerosis. Neurology, 1988, 38(10), 1631–4.
[848] Patten, SB; Neutel, CI. Corticosteroid-induced adverse psychiatric effects. Drug Saf, 2000, 22(2), 111–22.
[849] Chau, SY; Mok, CC. Factors predictive of corticosteroidpsychosis in patients with systemic lupus erythematosus. Neurology, 2003, 61(1), 104–7.
[850] Keenan, P; Jacobson, M; Soleymani, R; et al. The effect onmemory of chronic prednisone treatment in patients withsystemic disease. Neurology, 1996, 47((6), 1396–402.
[851] Trikudanathan, S; McMahon, GT. Optimum managementof glucocorticoid treated patients. Nat Rev Endocrinol, 2008, 4, 62–271.
[852] Souverein, P; Berars, A; Van Staa, T. Use of oral glucocorticoids and risk of cardiovascular and cerebrovasculardisease in a population based case-control study. Heart, 2004, 90(8), 859–65.
[853] Lehman, JS; Murrell, DF; Camilleri, MJ; Kalaaji, AN. Infection and infection prevention in patients treated with immunosuppressive medications for autoimmune bullous disorders. Dermatol Clin, 2011, 29, 591–8.
[854] LoCascio, V; Bonucci, E; Imbimbo, B; et al. Boneloss in response to long-term glucocorticoid therapy. Bone Miner, 1990, 8(1), 39–51.
[855] Canalis, E; Mazziotti, G; Giustina, A; Bilezikian, JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy. Osteoporos Int, 2007, 18, 1319–28.
[856] Weinstein, RS; Nicholas, RW; Manolagas, SC. Apoptosis of osteocytes in glucocorticoid- induced osteonecrosis of the hip. J Clin Endocrinol Metab, 2000, 85(8), 2907.
[857] Jia, D; O’Brien, CA; Stewart, SA; Manolagas, SC; Weinstein, RS. Glucocorticoids act directly on osteoclasts to increase their life span and reduce bonedensity. Endocrinology, 2006, 147(12), 5592–9.
[858] Hahn, TJ; Halstead, LR; Baran, DT. Effects off short term glucocorticoid administration on intestinal calcium absorption and circulating vitamin D metabolite concentrations in man. J Clin Endocrinol Metab, 1981, 52(1), 111–5.
[859] Suzuki, Y; Ichikawa, Y; Saito, E; Homma, M. Importance of increased urinary calcium excretion in the development of secondary hyperparathyroidism of patients under glucocorticoid therapy. Metabolism, 1983, 32(2), 151–6.
[860] Bonadonna, S; Burattin, A; Nuzzo, M; et al. Chronicglucocorticoid treatment alters spontaneous pulsatileparathyroid hormone secretory dynamics in humansubjects. Eur J Endocrinol, 2005, 152, 199–205.
[861] Lombardi, G; Colarusso, S; Di Somma, C; Guerra, E; Tauchmanova, L; Colao, A. The role of growthhormone in glucocorticoid-induced osteoporosis. J Endocrinol Invest, 2008, 31(7 Suppl), 38–42.
[862] Pearce, G; Tabensky, DA; Delmas, PD; Baker, HW; Seeman, E. Corticosteroid-induced bone loss in men. J Clin Endocrinol Metab, 1998, 83(3), 801.
[863] Van Staa, TP; Laan, RF; Barton, IP; Cohen, S; Reid, DM; Cooper, C. Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoid therapy. Arthritis Rheum, 2003, 48(11), 3224–9.
[864] van Staa, TP; Leufkens, HGM; Cooper, C. The epidemiology of corticosteroid-induced osteoporosis: a metaanalysis. Osteoporos Int, 2002, 13, 777–87.
[865] Van Staa, TP; Leufkens, HG; Abenhaim, L; Zhang, B; Cooper, C. Use of oral corticosteroids and risk of fractures. J Bone Miner Res, 2000, 15(6), 993–1000.
[866] Scully, C; Paes de Almedia, O; Porter, SR; et al. Pemphigus vulgaris: the manifestations and long-term management of 55 patients with oral lesions. Br J Dermatol, 1999, 140, 84–9.
[867] Grossman, JM; Gordon, R; Ranganath, VK; et al. American College of Rheumatology 2010 recommendations for the prevention and treatment of glucocorticoid- induced osteoporosis. Arthritis Care Res (Hoboken), 2010, 62(11), 1515–26.
[868] Cruse, LM; Valeriano, J; Vasey, FB; et al. Prevalence of evaluation and treatment of glucocorticoid-induced osteoporosis in men. J Clin Rheumatol, 2006, 12(5), 221–5.
[869] Feldstein, AC; Elmer, PJ; Nichols, GA; Herson, M. Practice patterns in patients at risk for glucocorticoidinducedosteoporosis. Osteoporos Int, 2005, 16(12), 2168–74.
[870] Homik, J; Suarez-Almazor, ME; Shea, B; et al. Calcium and vitamin D for corticosteroid-induced osteoporosis. Cochrane Database Syst Rev, 2000, 2, CD000952.
[871] Wang, L; Manson, JE; Sesso, HD. Calcium intake andrisk of cardiovascular disease: a review of prospective studies and randomized clinical trials. Am J Cardiovasc Drugs, 2012, 12(2), 105–16.
[872] Richy, F; Ethgen, O; Bruyere, O; et al. Efficacy of alphacalcidol and calcitriol in primary andcorticosteroid- induced osteoporosis: a meta-analysisof their effects on bone mineral density and fracturerate. Osteoporos Int, 2004, 15(4), 301–10.
[873] Sambrook, PN; Kotowicz, M; Nash, P; et al. Prevention and treatment of glucocorticoid-induced osteoporosis: a comparison of calcitriol, vitamin D plus calcium, and alendronate plus calcium. J Bone Miner Res, 2003, 18(5), 919–24.
[874] de Nijs, RN; Jacobs, JW; Lems, WF; et al. Alendronate or alfacalcidol in glucocorticoid-induced osteoporosis. N Engl J Med, 2006, 355(7), 675–84.
[875] Kanis, JA; Borgstrom, F; De Laet, C; et al. Assessment of fracture risk. Osteoporos Int, 2005, 16, 581–9.
[876] Siris, ES; Chen, YT; Abbott, TA; et al. Bone mineraldensity thresholds for pharmacological interventionto prevent fractures. Arch Intern Med, 2004, 164(10), 1108–12.
[877] The International Society for Clinical Densitometry, International Osteoporosis Foundation. 2010 official positions on FRAX. ( pdfs/Official%20Positions%20ISCD-IOF%20FRAX.pdf).
[878] Tosteson, AN; Melton 3rd, LJ; Dawson-Hughes, B; et al. Cost-effective osteoporosis treatment thresholds: the United States perspective. Osteoporos Int, 2008, 19(4), 437–47.
[879] Kanis, JA; Borgstrom, F; Zethraeus, N; et al. Interventionthresholds for osteoporosis in the UK. Bone, 2005, 36(1), 22–32.
[880] Kanis, JA; Borgstrom, F; Johnell, O; et al. Costeffectiveness of risedronate for the treatment of osteoporosisand prevention of fractures in postmenopausalwomen. Osteoporos Int, 2004, 15(11), 862–71.
[881] Borgstrom, F; Johnell, O; Kanis, JA; et al. Cost effectivenessof raloxifene in the treatment of osteoporosisin Sweden: an economic evaluation based on theMORE study. Pharmacoeconomics, 2004, 22(17), 1153–65.
[882] Saag, KG; Emkey, R; Schnitzer, TJ; et al. Alendronate for the prevention and treatment of glucocorticoid induced osteoporosis. Glucocorticoid-Induced Osteoporosis Intervention Study Group. N Engl J Med, 1998, 339(5), 292–9.
[883] Homik, J; Cranney, A; Shea, B; et al. Bisphosphonates for steroid induced osteoporosis. Cochrane Database Syst Rev, 2000, (2), CD001347.
[884] Plotkin, LI; Weinstein, RS; Parfitt, AM; et al. Preventionof osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin. J Clin Invest, 1999, 104, 1363–74.
[885] Weinstein, RS; Chen, JR; Powers, CC; et al. Promotion of osteoclast survival and antagonism of bisphosphonate- induced osteoclast apoptosis by glucocorticoids. J Clin Invest, 2002, 109, 1041–8.
[886] Wang, J; Stern, PH. Dose-dependent differential effects of risedronate on gene expression in osteoblasts. Biochem Pharmacol, 2011, 81(8), 1036–42.
[887] Brown, JP; Kendler, DL; McClung, MR; et al. The efficacy and tolerability of risedronate once a week forthe treatment of postmenopausal osteoporosis. Calcif Tissue Int, 2002, 71(2), 103–11.
[888] Reid, DM; Hughes, RA; Laan, RF; et al. Efficacy andsafety of daily risedronate in the treatment ofcorticosteroid- induced osteoporosis in men andwomen: a randomized trial. European Corticosteroid-Induced Osteoporosis Treatment Study. J Bone MinerRes, 2000, 15, 1006–113.
[889] Reid, DM; Devogelaer, JP; Saag, K; et al. Zoledronicacid and risedronate in the prevention and treatmentof glucocorticoid-induced osteoporosis (HORIZON): a multicenter, double-blind, double-dummy, randomizedcontrolled trial. Lancet, 2009, 373, 1253–63.
[890] Agrawal, Krueger DC; Engelke, JA; et al. Between mealrisedronate does not alter bone turnover in nursinghome residents. J Am Geriatr Soc, 2006, 54(5), 790–5.
[891] Bauer, DC; Black, D; Ensrud, K; et al. Upper gastrointestinaltract safety profile of alendronate: the fractureintervention trial. Arch Intern Med, 2000, 160(4), 517–25.
[892] Cardwell, CR; Abnet, CC; Cantwell, MM; et al. Exposure to oral bisphosphonates and risk of esophagealcancer. JAMA, 2010, 304, 657–63.
[893] Khosla, S; Burr, D; Cauley, J; et al. Bisphosphonate associated osteonecrosis of the jaw: report of a taskforce of the American Society for Bone and MineralResearch. J Bone Miner Res, 2007, 22(10), 1479–91.
[894] Odvina, CV; Zerwekh, JE; Rao, DS; et al. Severely suppressed bone turnover: a potential complication of alendronate therapy. J Clin Endocrinol Metab, 2005, 90(3), 1294–301.
[895] Park-Wyllie, LY; Mamdani, MM; Juurlink, DN; et al. Bisphosphonate use and the risk of subtrochanteric or femoral shaft fractures in older women. JAMA, 2011, 305(8), 783–9.
[896] Bone, HG; Hosking, D; Gevogelaer, JP; et al. Ten years’ experience with alendronate for osteoporosis in postmenopausalwomen. N Engl J Med, 2004, 350, 1189–99.
[897] Whitaker, M; Guo, J; Kehoe, T; et al. Bisphosphonatesfor osteoporosis—where do we go from here? N Engl J Med, 2012, 366, 2048–51.
[898] Khosla, S; Bilezikian, JP; Dempster, DW; et al. Benefitsand risks of bisphosphonate therapy for osteoporosis. J Clin Endocrinol Metab, 2012, 97(7), 2272–82.
[899] Lane, NE; Sanchez, S; Modin, GW; et al. Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlledclinical trial. J Clin Invest, 1998, 102, 1627–33.
[900] Compston, JE. Skeletal actions of intermittent parathyroidhormone: effects on bone remodeling andstructure. Bone, 2007, 40, 1447–52.
[901] Saag, KG; Shane, E; Boonen, S; et al. Teriparatide oralendronate in glucocorticoid-induced osteoporosis. N Engl J Med, 2007, 357, 2028–39.
[902] Saag. KG; Zanchetta. JR; Devogelaer. JP; et al. Effects of teriparatide versus alendronate for treating glucocorticoid-induced osteoporosis: thirty-six month results of a randomized, double-blind, controlled trial. Arthritis Rheum, 2009, 60, 3346–55.
[903] Murad, MH; Drake, MT; Mullan, RJ; et al. Comparative effectiveness of drug treatments to prevent fragility fractures: a systematic review and network metaanalysis. J Clin Endocrinol Metab, 2012, 97(6), 1871–90.
[904] Sambrook, PN; Birmingham, J; Kelly, P; et al. Prevention of corticosteroid osteoporosis: a comparison of calcium, calcitriol, and calcitonin. N Engl JMed, 1993, 328, 1747–52.
[905] Luengo, M; Pons, F; Martinez de Osaba, JM; et al. Prevention of further bone mass loss by nasal calcitoninin patients on long term glucocorticoid therapy forasthma: a two year follow up study. Thorax, 1994, 49, 1099–102.
[906] Cranney, A; Welch, V; Adachi, JD; et al. Calcitonin for the treatment and prevention of corticosteroid-induced osteoporosis Cochrane review. In: The Cochrane library. Issue 2. Oxford: Update Software, 2000.
[907] Bolognese, MA; Teglbjaerg, CD; Zanchetta, JR; et al. Denosumab significantly increases DXA BMD atboth trabecular and cortical sites: results from the FREEDOM study. J Clin Densitom, 2013, 16(2), 147–53.
[908] Dore, RK; Cohen, SB; Lane, NE; et al. Effects of denosumab on bone mineral density and bone turnover in patients with rheumatoid arthritis receiving concurrent glucocorticoids or bisphosphonates. Ann Rheum Dis, 2010, 69, 872–5.
[909] Cummings, SR; Karpf, DB; Harris, F; et al. Improvement in spine bone density and reduction in risk of vertebral fractures during treatment with antiresorptive drugs. Am J Med, 2002, 112(4), 281–9.
[910] Lenchik, L; Keibzak, GM; Blunt, BA; et al. What is the role of serial bone mineral density measurements inpatient management? J Clin Densitom, 2002, 5, S29–38.
[911] Binkley, N; Bilezikian, JP; Kendler, DL; et al. Official positions of the International Society for Clinical Densitometry and Executive Summary of the 2005 position development conference. J Clin Densitom, 2006, 9, 4–14.
[912] Clore, JN; Thurby-Hay, L. Glucocorticoid-induced hyperglycemia. Endocr Pract, 2009, 15(5), 469–74.
[913] Gurwitz, JH. Glucocorticoids and the risk for initiation of hypoglycemic therapy. Arch Intern Med, 1994, 154(1), 97–101.
[914] Lansang, MC; Hustak, LK. Glucocorticoid-induced diabetesand adrenal suppression: how to detect and managethem. Cleve Clin J Med, 2011, 78(11), 748–56.
[915] Hoogwerf, B; Danese, RD. Drug selection and themanagement of corticosteroid-related diabetes mellitus. Rheumatol Dis Clin N Am, 1999, 25(3), 489–505.
[916] Hoogwerf, BJ; Goetz, FC. Urinary C-peptide: a simplemeasure of integrated insulin production with emphasison the effects of body size, diet, and corticosteroids. J Clin Endocrinol Metab, 1983, 56(1), 60–7.
[917] Ceriello, A. Oscillating glucose is more deleteriousto endothelial function and oxidative stress thanmean glucose in normal and type 2 diabetic patients. Diabetes, 2008, 57(5), 1349–54.
[918] Campbell, IW. Epidemiology and clinical presentation of type 2 diabetes. Value Health, 2000, 3 Suppl 1, 3–6.
[919] American Diabetes Association. Standards of medicalcare in diabetes—2012. Diabetes Care, 2012, 35 Suppl1, S11–63.
[920] Moleiro, S. Atypical response to treatment in linearIgA bullous dermatosis of childhood: revision of literature. Dermatol Online J, 2011, 17(6), 5.
[921] Trence, DL; Hirsch, IB. Hyperglycemic crises in diabetesmellitus type 2. Endocrinol Metab Clin North Am, 2001, 30(4), 817–31.
[922] Davidson, J. New-onset diabetes after transplantation: 2003 International consensus guidelines. Proceedings of an international expert panel meeting. Barcelona, Spain, 19 February 2003. Transplantation, 2003, 75(10), SS3–24.
[923] Attaway, A; Mersfelder, TL; Vaishnav, S; Baker, JK. Bullous pemphigoid associated with dipeptidyl peptidase IV inhibitors. A case report and review of literature. J Dermatol Case Rep, 2014, 8(1), 24-8.
[924] Gerstein, HC. Effects of intensive glucose loweringin type 2 diabetes. N Engl J Med, 2008, 358(24), 2545–59.
[925] Wysocki, AB. Evaluating and managing open skin wounds: colonization versus infection. AACN Clin Issues, 2002, 13(3), 382–97.
[926] Clay, T; Pandya, AG. Minimizing complications in autoimmune blistering diseases. Dermatol Clin, 2011, 29, 577–83.
[927] Altemus, M; Rao, B; Dhabhar, FS; Ding, W; Granstein RD. Stress-induced changes in skin barrier function in healthy women. J Invest Dermatol, 2001, 117(2), 309–17.
[928] Belgnaoui, FZ; Senouci, K; Chraibi, H; et al. Predisposition to infection in patients with pemphigus. Retrospective study of 141 cases. Presse Med, 2007, 36(11 Pt 1), 1563–9.
[929] Langan, SM; Hubbard, R; Fleming, K; et al. A population-based study of acute medical conditions associated with bullous pemphigoid. Br J Dermatol, 2009, 161(5), 1149–52.
[930] Savin, JA; Noble, WC. Immunosuppression and skin infection. Br J Dermatol, 1975, 93(1), 115–20.
[931] Robson, MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin N Am, 1997, 77(3), 637–50.
[932] Boughrara, Z; Ingen-Housz-Oro, S; Legrand, P; et al. Cutaneous infections in bullous pemphigoid patients treated with topical corticosteroids. Ann Dermatol Venereol, 2010, 137(5), 345–51.
[933] Tirado-Sánchez, A; Bonifaz, A; Ponce-Olivera, RM. Increasing prevalence of antimicrobial resistance among gram-negative isolates in patients with pemphigus vulgaris. J Am Acad Dermatol, 2014, 66, e16-8.
[934] Feldmeyer, L; Trüeb, RM; French, LE; et al. Pitfall: pemphigus herpeticatus should not be confounded with resistant pemphigus vulgaris. J Dermatol Treat, 2010, 21(5), 311–3.
[935] Nikkels, AF; Delvenne, P; Herfs, M; et al. Occult herpessimplex virus colonization of bullous dermatitides. Am J Clin Dermatol, 2008, 9(3), 163–8.
[936] Avalos-Peralta, P; Herrera, A; Rios-Martin, JJ; et al. Localized Kaposi’s sarcoma in a patient with pemphigusvulgaris. J Eur Acad Dermatol Venereol, 2006, 20(1), 79–83.
[937] Adachi, M; Tsuruta, D; Imanishi, H; et al. Necrotizing fasciitis caused by Cryptococcus neoformans in apatient with pemphigus vegetans. Clin Exp Dermatol, 2009, 34(8), e751–3.
[938] Yoo, SS; Tran, M; Anhalt, G; et al. Disseminatedcellulitic cryptococcosis in the setting of prednisone monotherapy for pemphigus vulgaris. J Dermatol, 2003, 30(5), 405–10.
[939] Uslan, DZ; Kowalski, TJ; Wengenack, NL; et al. Skin and soft tissue infections due to rapidly growing mycobacteria: comparison of clinical features, treatment, and susceptibility. Arch Dermatol, 2006, 142(10), 287–92.
[940] Kawabata, E; Morita, K; Matsuyoshi, N; et al. Bilateral inguinal scrofuloderma during steroid therapy in a patient with bullous pemphigoid. J Dermatol, 1995, 22(8), 582–6.
[941] Steele, RW. Should immunocompromised patients have pets? Ochsner J, 2008, 8(3), 134–9.
[942] Fiore, AE; Uyeki, TM; Broder, K; et al. General recommendationson immunization—recommendations ofthe Advisory Committee on Immunization Practices (ACIP). National Center for Immunization and Respiratory Diseases. MMWR Recomm Rep, 2011, 60(2), 1–64.
[943] Harpaz, R; Ortega-Sanchez, IR; Seward, JF. Advisory Committee on Immunization Practices (ACIP), Centers for Disease Control and Prevention (CDC). Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep, 2008, 57(RR-5), 1–30.
[944] Huang, JT; Rademaker, A; Paller, AS. Dilute bleachbaths for Staphylococcus aureus colonization inatopic dermatitis to decrease disease severity. Arch Dermatol, 2011, 147(2), 246–7.
[945] Craig, FE; Smith, EV; Williams, HC. Bleach baths to reduce severity of atopic dermatitis colonized by Staphylococcus. Arch Dermatol, 2010, 146(5), 541–3.
[946] Gerhart, JL; Kalaaji, AN. Development of Pneumocystiscarinii pneumonia in patients with immunobullous and connective tissue disease receiving immune suppressive medications. J Am Acad Dermatol, 2010, 62(6), 957–61.
[947] Lehman, JS; Kalaaji, AN. Role of primary prophylaxisfor pneumocystis pneumonia in patients treated withsystemic corticosteroids or other immune suppressive agents for immune-mediated dermatologic conditions. J Am Acad Dermatol, 2010, 63(5), 815–23.
[948] Calne, RY. The rejection of renal homografts. Inhibitionin dogs by 6-mercaptopurine. Lancet, 1960, 1, 417–8.
[949] Elion, GB. The purine path to chemotherapy. Science, 1989, 244, 41–7.
[950] Calne, RY. Renal transplantation in man: a report of five cases, using cadaveric donors. Br Med J, 1963, 2, 645–51.
[951] Karran, P; Attard, N. Thiopurines in current medical practice: molecular mechanisms and contributions totherapy-related cancer. Nat Rev Cancer, 2008, 8, 24–36.
[952] Szawlowski, PW. Azathioprine suppresses themixed lymphocyte reaction of patients with Lesch-Nyhan syndrome. Br J Clin Pharmacol, 1985, 20, 489–91.
[953] Uchiyama, K. Thiopurine S-methyltransferase and inosine triphosphate pyrophosphohydrolasegenes in Japanese patients with infl ammatory boweldisease in whom adverse drug reactions were induced by azathioprine/6-mercaptopurine treatment. J Gastroenterol, 2009, 44, 197–203.
[954] Aarbakke, J. Thiopurine biology and pharmacology. Trends Pharmacol Sci, 1997, 18, 3–7.
[955] Tiede, I. CD28-dependent Rac1 activation is themolecular target of azathioprine in primary human CD4+T lymphocytes. J Clin Invest, 2003, 111, 1133–45.
[956] Marinkovic, G. Inhibition of GTPase Rac1 in endothelium by 6-mercaptopurine results in immunosuppression in nonimmune cells: new target for an olddrug. J Immunol, 2014, 192, 4370–8.
[957] Yamamoto, H. NF-kappaB activation in CD27 signaling: involvement of TNF receptor-associatedfactors in its signaling and identification of functionalregion of CD27. J Immunol, 1998, 161, 4753–9.
[958] Aldinucci, A. Modulating dendritic cells (DC) from immunogenic to tolerogenic responses: a novelmechanism of AZA/6-MP. J Neuroimmunol, 2010, 218, 28–35.
[959] Krakowski, A. Pemphigus vulgaris. Arch Dermatol, 1969, 100, 117.
[960] Wolff, K; Schreiner, E. Immunosuppressive therapy of pemphigus vulgaris. Preliminary results of azathioprine (Imuran) treatment). Arch Klin Exp Dermatol, 1969, 235, 63–77.
[961] Beissert, S; Mimouni, D; Kanwar, AJ; Solomons, N; Kalia, V; Anhalt, GJ. Treating pemphigus vulgaris with prednisone and mycophenolate mofetil: a multicenter, randomized, placebo-controlled trial. J Invest Dermatol, 2010, 130, 2041–8.
[962] Beissert, S; Werfel, T; Frieling, U; et al. A comparison of oral methylprednisolone plusazathioprine or mycophenolate mofetil for the treatmentof pemphigus. Arch Dermatol, 2006, 142, 1447–54.
[963] Chams-Davatchi, C. Randomized double blindtrial of prednisolone and azathioprine, vs. prednisoloneand placebo, in the treatment of pemphigus vulgaris. J Eur Acad Dermatol Venereol, 2013, 27, 1285–92.
[964] Zillikens, D. IgA pemphigus foliaceus: a case report. Dermatologica, 1990, 181, 304–7.
[965] Frew, JW; Murrell, DF. Current management strategies in paraneoplastic pemphigus (paraneoplastic autoimmunemultiorgan syndrome). Dermatol Clin, 2011, 29, 607–12.
[966] Lam, S. Paraneoplastic pemphigus, cicatricial conjunctivitis, and acanthosis nigricans with pachydermatoglyphyin a patient with bronchogenic squamous cellcarcinoma. Ophthalmology, 1992, 99, 108–13.
[967] Verrinim A. A patient with immunological featuresof paraneoplastic pemphigus in the absence of a detectablemalignancy. Acta Derm Venereol, 2002, 82, 382–4.
[968] Behzad, M; Möbs, C; Kneisel, A; et al. Combined treatmentwith immunoadsorption and rituximab leads tofast and prolonged clinical remission in difficult-to-treat pemphigus vulgaris. Br J Dermatol, 2012, 166, 844–52.
[969] Ostensen, M. Treatment with immunosuppressive anddisease modifying drugs during pregnancy and lactation. Am J Reprod Immunol, 1992, 28, 148–52.
[970] Janssen, NM; Genta, MS. The effects of immunosuppressiveand anti-infl ammatory medications on fertility, pregnancy, and lactation. Arch Intern Med, 2000, 160, 610–9.
[971] Tendron, A. In utero exposure to immunosuppressive drugs: experimental and clinical studies. Pediatr Nephrol, 2002, 17, 121–30.
[972] Marder, W. In utero azathioprine exposure andincreased utilization of special educational services in children born to mothers with systemic lupus erythematosus. Arthr Care Res (Hoboken), 2013, 65, 759–66.
[973] Tichy M. Life-threatening course of pemphigusvulgaris complicated by sepsis caused by azathioprine induced bone marrow suppression: successfully managedwith combination therapy. Dermatol Ther 2014, 27,183–6.
[974] Anstey, A. Pancytopenia related to azathioprine—an enzyme deficiency caused by a commongenetic polymorphism: a review. J R Soc Med, 1992, 85, 752–6.
[975] Otterness, D. Human thiopurine methyltransferaseharmacogenetics: gene sequence polymorphisms. Clin Pharmacol Ther, 1997, 62, 60–73.
[976] Kumagai, K. Allelotype frequency of the thiopurine methyltransferase (TPMT) gene in Japanese. Pharmacogenetics, 2001, 11, 275–8.
[977] Lennard, L. Pharmacogenetics of acute azathioprine toxicity: relationship to thiopurine methyltransferase genetic polymorphism. Clin Pharmacol Ther, 1989, 46, 149–54.
[978] Sumi, S. Genetic basis of inosine triphosphatepyrophosphohydrolase deficiency. Hum Genet, 2002, 111, 360–7.
[979] Carney, DM. Massive azathioprine overdose. Case report and review of the literature. Am J Med, 1974, 56, 133–6.
[980] Mahmood, K. Intentional overdose of azathioprinein a patient with systemic lupus erythematosus. Scott Med J, 2013, 58, e3–4.
[981] Silman, AJ. Lymphoproliferative cancer and other malignancy in patients with rheumatoid arthritistreated with azathioprine: a 20 year follow up study. Ann Rheum Dis, 1988, 47, 988–92.
[982] Pasternak, B. Use of azathioprine and the risk of cancer in inflammatory bowel disease. Am J Epidemiol, 2013, 177, 1296–305.
[983] Khan, N. Risk of lymphoma in patients with ulcerativecolitis treated with thiopurines: a nationwide retrospective cohort study. Gastroenterology, 2013, 145, 1007–15.
[984] Pedersen, EG. Risk of non-melanoma skin cancerin myasthenia patients treated with azathioprine. Eur J Neurol, 2014, 21, 454–8.
[985] Pedersen, EG. Use of azathioprine for nonthymomamyasthenia and risk of cancer: a nationwide case-control study in Denmark. Eur J Neurol, 2013, 20, 942–8.
[986] van den Reek, JM. Increased incidence of squamous cell carcinoma of the skin after long-term treatment with azathioprine in patients with auto-immune inflammatory rheumatic diseases. J Eur Acad Dermatol Venereol, 2014, 28, 27–33.
[987] Ramsay, HM. Non-melanoma skin cancer risk in the Queensland Renal transplant population. Br J Dermatol, 2002, 147, 950–6.
[988] O’Donovan, P. Azathioprine and UVA light generate mutagenic oxidative DNA damage. Science, 2005, 309, 1871–4.
[989] Hemmens, VJ; Moore, DE. Photochemical sensitizationby azathioprine and its metabolites—I.6- Mercaptopurine. Photochem Photobiol, 1986, 43, 247–55.
[990] Reeve, VE. Effect of immunosuppressive agents and sunscreens on UV carcinogenesis in the hairless mouse. Aust J Exp Biol Med Sci, 1985, 63(Pt 6), 655–65.
[991] Allison, AC. Mechanisms of action of mycophenolate mofetil. Lupus, 2005, 14 Suppl 1, s2–8.
[992] Allison, AC; Eugui, EM. Immunosuppressive and other effects of mycophenolic acid and an ester prodrug, mycophenolate mofetil. Immunol Rev, 1993, 136, 5–28.
[993] Carr, SF; Papp, E; Wu, JC; Natsumeda, Y. Characterization of human type I and type II IMP dehydrogenases. J Biol Chem, 1993, 268, 27286–90.
[994] Allison, AC; Eugui, EM. Mycophenolate mofetil andits mechanisms of action. Immunopharmacology, 2000, 47, 85–118.
[995] Cohn, RG; Mirkovich, A; Dunlap, B; Burton, P; Chiu, SH; Eugui, E; Caulfield, JP. Mycophenolic acid increases apoptosis, lysosomes and lipid droplets in human lymphoid and monocytic cell lines. Transplantation, 1999, 68, 411–8.
[996] Allison, AC; Almquist, SJ; Muller, CD; Eugui, EM. In vitro immunosuppressive effects of mycophenolic acid and an ester pro-drug, RS-61443. Transplant Proc, 1991, 23, 10–4.
[997] Blaheta, RA; Leckel, K; Wittig, B; et al. Mycophenolate mofetil impairs transendothelialmigration of allogeneic CD4 and CD8T-cells. Transplant Proc, 1999, 31, 1250–2.
[998] Morath, C; Schwenger, V; Beimler, J; Mehrabi, A; Schmidt, J; Zeier, M; Muranyi, W. Antifibrotic actions of mycophenolic acid. Clin Transplant, 2006, 20 Suppl 17, 25–9.
[999] Colic, M; Stojic-Vukanic, Z; Pavlovic, B; Jandric, D; Stefanoska, I. Mycophenolate mofetil inhibits differentiation, maturation and allostimulatory function ofhuman monocyte-derived dendritic cells. Clin Exp Immunol, 2003, 134, 63–9.
[1000] Lagaraine, C; Lebranchu, Y. Effects of immunosuppressivedrugs on dendritic cells and tolerance induction. Transplantation, 2003, 75, 37S–42.
[1001] Senda, M; DeLustro, B; Eugui, E; Natsumeda, Y. Mycophenolic acid, an inhibitor of IMP dehydrogenase that is also an immunosuppressive agent, suppressesthe cytokine-induced nitric oxide production in mouseand rat vascular endothelial cells. Transplantation, 1995, 60, 1143–8.
[1002] Bullingham, R; Monroe, S; Nicholls, A; Hale, M. Pharmacokinetics and bioavailability of mycophenolatemofetil in healthy subjects after single-doseoral and intravenous administration. J Clin Pharmacol, 1996, 36, 315–24.
[1003] Sweeney, MJ. Mycophenolic acid and its mechanismof action in cancer and psoriasis. Jpn J Antibiot, 1977, 30(Suppl), 85–92.
[1004] Bullingham, RE; Nicholls, AJ; Kamm, BR. Clinical pharmacokinetics of mycophenolate mofetil. Clin Pharmacokinet, 1998, 34, 429–55.
[1005] Behrend, M. Adverse gastrointestinal effects of mycophenolatemofetil: aetiology, incidence and management. Drug Saf, 2001, 24, 645–63.
[1006] Goldblum, R. Therapy of rheumatoid arthritis with mycophenolate mofetil. Clin Exp Rheumatol., 1993, 11Suppl 8, S117–9.
[1007] Mimouni, D; Anhalt, GJ; Cummins, DL; Kouba, DJ;Thorne, JE; Nousari, HC. Treatment of pemphigus vulgaris and pemphigus foliaceus with mycophenolatemofetil. Arch Dermatol, 2003, 139, 739–42.
[1008] Bjarnason, I. Enteric coating of mycophenolatesodium: a rational approach to limit topical gastrointestinallesions and extend the therapeutic index ofmycophenolate. Transplant Proc, 2001, 33, 3238–40.
[1009] Salvadori, M; Holzer, H; de Mattos, A; Sollinger, H; Arns, W; Oppenheimer, F; Maca, J; Hall, M. Enteric coated mycophenolate sodium is therapeuticallyequivalent to mycophenolate mofetil in de novo renaltransplant patients. Am J Transplant, 2004, 4, 231–6.
[1010] Budde, K; Curtis, J; Knoll, G; Chan, L; Neumayer, HH; Seifu, Y; Hall, M. Enteric-coated mycophenolatesodium can be safely administered in maintenance renal transplant patients: results of a 1-year study. Am J Transplant, 2004, 4, 237–43.
[1011] Kobashigawa, JA; Renlund, DG; Gerosa, G; et al. Similar efficacy and safety of entericcoatedmycophenolate sodium (EC-MPS, myfortic)compared with mycophenolate mofetil (MMF) in denovo heart transplant recipients: results of a 12-month, single-blind, randomized, parallel-group, multicenter study. J Heart Lung Transplant, 2006, 25, 935–41.
[1012] Chan, L; Mulgaonkar, S; Walker, R; Arns, W; Ambuhl, P; Schiavelli R. Patient-reported gastrointestinal symptomburden and health-related quality of life following conversionfrom mycophenolate mofetil to enteric-coatedmycophenolate sodium. Transplantation, 2006, 81, 1290–7.
[1013] Sabbatini, M; Capone, D; Gallo, R; et al. EC-MPS permits lower gastrointestinal symptom burden despite higher MPA exposure in patients with severe MMF-related gastrointestinal side-effects. Fundam Clin Pharmacol, 2009, 23, 617–24.
[1014] Engelen, W; Verpooten, GA; Van der Planken, M; Helbert, MF; Bosmans, JL; De Broe, ME. Four cases ofred blood cell aplasia in association with the use ofmycophenolate mofetil in renal transplant patients. Clin Nephrol, 2003, 60, 119–24.
[1015] Arbeiter, K; Greenbaum, L; Balzar, E; Muller, T; Hofmeister, F; Bidmon, B; Aufricht, C. Reproducible erythroid aplasia caused by mycophenolate mofetil. Pediatr Nephrol, 2000, 14, 195–7.
[1016] Mydlarski, PR. Mycophenolate mofetil: a dermatologicperspective. Skin Therapy Lett, 2005, 10, 1–6.
[1017] Epinette, WW; Parker, CM; Jones, EL; Greist, MC. Mycophenolic acid for psoriasis. A review of pharmacology, long-term efficacy, and safety. J Am Acad Dermatol, 1987, 17, 962–71.
[1018] Simmons, WD; Rayhill, SC; Sollinger, HW. Preliminary risk-benefit assessment of mycophenolate mofetil in transplant rejection. Drug Saf, 1997, 17, 75–92.
[1019] Hambach, L; Stadler, M; Dammann, E; Ganser, A; Hertenstein, B. Increased risk of complicated CMV infection with the use of mycophenolate mofetil inallogeneic stem cell transplantation. Bone Marrow Transplant, 2002, 29, 903–6.
[1020] Sarmiento, JM; Dockrell, DH; Schwab, TR; Munn, SR; Paya, CV. Mycophenolate mofetil increases cytomegalovirusinvasive organ disease in renal transplantpatients. Clin Transplant, 2000, 14, 136–8.
[1021] ter Meulen, CG; Wetzels, JF; Hilbrands, LB. The influence of mycophenolate mofetil on the incidence andseverity of primary cytomegalovirus infections anddisease after renal transplantation. Nephrol DialTransplant, 2000, 15, 711–4.
[1022] Weber, SC; Uhlenberg, B; Raile, K; Querfeld, U; Muller, D. Polyoma virus-associated progressive multifocal leukoencephalopathy after renal transplantation: regression following withdrawal of mycophenolate mofetil. Pediatr Transplant, 2011, 15, E19–24.
[1023] Manfro, RC; Vedolin, L; Cantarelli, M; Oppitz, P; Antunes, AC; Rieder, CR. Progressive multifocal leukoencephalopathyin a kidney transplant recipientafter conversion to mycophenolic acid therapy. Transpl Infect Dis, 2009, 11, 189–90.
[1024] Lefevre, G; Queyrel, V; Maurage, CA; et al. Effective immune restoration after immunosuppressant discontinuation in a lupus patient presenting progressive multifocal leukoencephalopathy. J Neurol Sci, 2009, 287, 246–9.
[1025] Kitchin, JE; Pomeranz, MK; Pak, G; Washenik, K; Shupack, JL. Rediscovering mycophenolic acid: a review of its mechanism, side effects, and potential uses. J Am Acad Dermatol, 1997, 37, 445–9.
[1026] Mathew, TH. A blinded, long-term, randomized multicenterstudy of mycophenolate mofetil in cadaveric renaltransplantation: results at three years. Tricontinental Mycophenolate Mofetil Renal Transplantation Study Group. Transplantation, 1998, 65, 1450–4.
[1027] Robson, R; Cecka, JM; Opelz, G; Budde, M; Sacks, S. Prospective registry-based observational cohort study of the long-term risk of malignancies in renaltransplant patients treated with mycophenolate mofetil. Am J Transplant, 2005, 5, 2954–60.
[1028] O’Neill, JO; Edwards, LB; Taylor, DO. Mycophenolate mofetil and risk of developing malignancy after orthotopic heart transplantation: analysis of the transplant registry of the International Society for Heart and Lung Transplantation. J Heart Lung Transplant, 2006, 25, 1186–91.
[1029] Lynch, WS; Roenigk, Jr HH. Mycophenolic acid for psoriasis. Arch Dermatol, 1977, 113, 1203–8.
[1030] Sifontis, NM; Coscia, LA; Constantinescu, S; Lavelanet, AF; Moritz, MJ; Armenti, VT. Pregnancy outcomes insolid organ transplant recipients with exposure tomycophenolate mofetil or sirolimus. Transplantation, 2006, 82, 1698–702.
[1031] Le Ray, C; Coulomb, A; Elefant, E; Frydman, R; Audibert, F. Mycophenolate mofetil in pregnancy afterrenal transplantation: a case of major fetal malformations. Obstet Gynecol, 2004, 103, 1091–4.
[1032] Tjeertes, IF; Bastiaans, DE; van Ganzewinkel, CJ; Zegers, SH. Neonatal anemia and hydrops fetalis aftermaternal mycophenolate mofetil use. J Perinatol, 2007, 27, 62–4.
[1033] Anderka, MT; Lin, AE; Abuelo, DN; Mitchell, AA; Rasmussen, SA. Reviewing the evidence for mycophenolatemofetil as a new teratogen: case report andreview of the literature. Am J Med Genet A, 2009, 149A, 1241–8.
[1034] Gimenez, F; Foeillet, E; Bourdon, O; Weller, S; Garret, C; Bidault, R; Singlas, E. Evaluation of pharmacokinetic interactions after oral administration of mycophenolate mofetil and valaciclovir or aciclovir to healthy subjects. Clin Pharmacokinet, 2004, 43, 685–92.
[1035] Jones, EL; Epinette, WW; Hackney, VC; Menendez, L; Frost, P. Treatment of psoriasis with oral mycophenolic acid. J Invest Dermatol, 1975, 65, 537–42.
[1036] Gomez, EC; Menendez, L; Frost, P. Efficacy of mycophenolicacid for the treatment of psoriasis. J AmAcad Dermatol, 1979, 1, 531–7.
[1037] Enk, AH; Knop, J. Mycophenolate is effective in the treatment of pemphigus vulgaris. Arch Dermatol, 1999, 135, 54–6.
[1038] Chams-Davatchi, C; Nonahal Azar, R; Daneshpazooh, M; et al. Open trial of mycophenolate mofetil in thetreatment of resistant pemphigus vulgaris. Ann Dermatol Venereol, 2002, 129, 23–5.
[1039] Esmaili, N; Chams-Davatchi, C; Valikhani, M; Farshidfar, F; Parvaneh, N; Tamizifar, B. Treatment of pemphigus vulgaris with mycophenolate mofetil as a steroid-sparing agent. Eur J Dermatol, 2008, 18, 159–64.
[1040] Grundmann-Kollmann, M; Korting, HC; Behrens, S; et al. Mycophenolate mofetil: a new therapeutic option inthe treatment of blistering autoimmune diseases. J Am Acad Dermatol, 1999, 40, 957–60.
[1041] Baskan, EB; Yilmaz, M; Tunali, S; Saricaoglu, H. Efficacy and safety of long-term mycophenolatesodium therapy in pemphigus vulgaris. J Eur Acad Dermatol Venereol, 2009, 23, 1432–4.
[1042] Williams, JV; Marks, Jr JG; Billingsley, EM. Use of mycophenolate mofetil in the treatment of paraneoplastic pemphigus. Br J Dermatol, 2000, 142, 506–8.
[1043] Zuidema, J; Hilbers-Modderman, ESM; Merkus, FWHM. Clinical pharmokinetics of dapsone. Clin Pharmacokinet, 1986, 11, 299–315.
[1044] May, DG; Arns, PA; Richards, WO; et al. The disposition of dapsone in cirrhosis. Clin Pharmacol Ther, 1992, 51, 689–700.
[1045] Caproni, M; Antiga, E; Melani, L; et al. Guidelines for the diagnosis and treatment of dermatitis herpetiformis. J Eur Acad Dermatol Venereol, 2009, 23, 633–8.
[1046] Zhu, YI; Stiller, MJ. Dapsone and sulfones in dermatology: overview and update. J Am Acad Dermatol, 2001, 45(3), 420–34.
[1047] Mentink, LF; de Jong, MC; Kloosterhuis, GJ; et al. Coexistence of IgA antibodies to desmogleins 1 and 3 inpemphigus vulgaris, pemphigus foliaceus and paraneoplastic pemphigus. Br J Dermatol, 2007, 156(4), 635–41.
[1048] Winkelmann, RK; Roth, HL. Dermatitis herpetiformis with acantholysis or pemphigus with response to sulfonamides: report of two cases. Arch Dermatol, 1960, 82, 385–90.
[1049] Basset, N; Guillot, B; Michel, B; et al. Dapsone as initialtreatment in superficial pemphigus. Report of nine cases. Arch Dermatol, 1987, 123(6), 783–5.
[1050] Beutner, EH; Chorzelski, TP; Wilson, RM; et al. IgA pemphigus foliaceus. J Am Acad Dermatol, 1989, 20, 89–97.
[1051] Niimi, Y; Kawana, S; Kusunoki, T. IgA pemphigus: acase report and its characteristic clinical features comparedto subcorneal pustular dermatosis. J Am Acad Dermatol, 2000, 43(3), 546–9.
[1052] Suzuki, M; Karaube, S; Kobori, Y; et al. IgA pemphigusoccurring in a 1-month-old infant. J Am Acad Dermatol, 2003, 48(2 Suppl), S22–4.
[1053] Hirata, Y; Abe, R; Kikuchi, K; et al. Intraepidermal neutrophilic IgA pemphigus successfully treated with dapsone. Eur J Dermatol, 2011, 22(2), 282–3.
[1054] Kishimoto, K; Iwatsuki, K; Akiba, H; et al. Subcorneal pustular dermatosis-type IgA pemphigus induced by thiol drugs. Eur J Dermatol, 2001, 11(1), 41–4.
[1055] Gniadecki, R; Bygum, A; Clemeensen, O; et al. IgA pemphigus: the first two Scandinavian cases. Acta Dermatol, 2002, 82(6), 441–5.
[1056] Monshi, B; Ritcher, L; Hashimoto, T; et al. IgA pemphigus of the subcorneal pustular dermatosis type: successful therapy with a combination of dapsone andacitretin. Hautartz, 2012, 63(6), 482–6. Only Abstract.
[1057] Jing, Z; Quan, T; Shu-Feng, Z. Clinical pharmacology of cyclophosphamide and ifosfamide. Curr Drug Ther, 2006, 1, 55–84.
[1058] Sethy, P; Khandpur, S; Sharma, V. Randomized open comparative trial of dexamethasone-cyclophosphamidepulse and daily oral cyclophosphamide versus cyclophosphamide pulse and daily oral prednisolone in pemphigus vulgaris. Indian J Dermatol Venereol Leprol, 2009, 75(5), 476–82.
[1059] Herzberg, MS; Schiffer, M; Sullivan, J; Stapleton, K. Paraneoplastic pemphigus in two patients with B-cell non-Hodgkin’s lymphoma: significant responses to cyclophosphamide and prednisolone. Am J Hematol, 2000, 63, 105–6.
[1060] Becker, LR; Bastian, BC; Wesselmann, U; Karls, A; Hamm, H; Bröker, EB. Paraneoplastic pemphigus treated with dexamethasone/cyclophosphamide pulse therapy. Eur J Derm, 1998, 8, 551–3.
[1061] Meurer, M. Immunosuppressive therapy for autoimmune bullous diseases. Clin Dermatol, 2012, 30, 78–83.
[1062] Monach, PA; Arnold, LM; Merkel, PA. Incidence and prevention of bladder toxicity from cyclophosphamide in the treatment of rheumatic diseases. Arthritis Rheum, 2010, 62(1), 9–21.
[1063] Schuchter, LM; Hensley, ML; Meropol, NJ; Winer, EP. 2002 update of recommendations for the use of chemotherapyand radiotherapy protectants: clinical practice guidelines of the American Society of Clinical Oncology. J Clin Oncol, 2002, 20(12), 2895–903.
[1064] Sneddon, IB. A clinical trial of tetracycline in rosacea. Br J Dermatol, 1966, 78(12), 649–52.
[1065] Monk, E; Shalita, A; Siegel, DM. Clinical applications of non-antimicrobial tetracyclines in dermatology. Pharmacol Res, 2011, 63(2), 130–45.
[1066] Viera, MH; Perez, OA; Berman, B. Incyclinide. Drugs Fut., 2007, 32(3), 209.
[1067] Bastos, FFS. Tetracyclines and Pain. Naunyn-Schmiedeberg’s Arch Pharmacol, 2012, 385(3), 225–41.
[1068] Dezube, BJ. Randomized phase II trial of matrix metalloproteinase inhibitor COL-3 in AIDS-relatedKaposi’s sarcoma: an AIDS malignancy consortium study. J Clin Oncol, 2006, 24(9), 1389–94.
[1069] Sapadin, AN; Fleischmajer, R. Tetracyclines: nonantibiotic properties and their clinical implications. J Am Acad Dermatol, 2006, 54(2), 258–65.
[1070] Fivenson, DP. Nicotinamide and tetracycline therapy of bullous pemphigoid. Arch Dermatol, 1994, 130(6), 753.
[1071] Ozog, DM. Minocycline-induced hyperpigmentationin patients with pemphigus and pemphigoid. Arch Dermatol, 2000, 136(9), 1133.
[1072] Fine, JD. Management of acquired bullous skin diseases. N Engl J Med, 1995, 333(22), 1475–84.
[1073] Wojnarowska, F. Guidelines for the managementof bullous pemphigoid. Br J Dermatol, 2002, 147(2), 214–21.
[1074] Kasperkiewicz, M; Schmidt, E. Current treatment of autoimmune blistering diseases. Curr Drug Discov Technol, 2009, 6(4), 270.
[1075] Bhatia, N. Use of antibiotics for noninfectious dermatologicdisorders. Dermatol Clin, 2009, 27(1), 85–9.
[1076] Gelfand, E. Differences between IGIV products: impact on clinical outcome. Int Immunopharmacol, 2006, 6, 592–9.
[1077] Frauger, E; Grassi, J; Pradel, V; et al. Use of intravenous immunoglobulins in clinical practice: data from three French university hospitals. Fund Clin Pharmacol, 2011, 25, 753–61.
[1078] Robinson, P; Anderson, D; Brouwers, M; Feasby, T; Hume, H. Evidence-based guidelines on the use of intravenous immune globulin for hematologic and neurologic conditions. Trans Med Rev, 2007, 21(2), S3–8.
[1079] Smith, S; Dennington, P; Cooper, A. Use of intravenous immunoglobulin for treatment of dermatological conditions in Australia: a review. Australas J Dermatol., 2010, 51, 227–37.
[1080] Sami, N; Bhol, K; Ahmed, A. Influence of IVIg therapy on autoantibody titers to desmoglein 1 in patients with pemphigus foliaceus. Clin Immunol, 2002, 105, 192–8.
[1081] Nousari, HC. Mycophenolate mofetil in autoimmuneand inflammatory skin disorders. J Am Acad Dermatol, 1999, 40(2), 265–8.
[1082] Lolis, M; Toosi, S; Czernick, A; Bystryn, J. Effect ofintravenous immunoglobulin with or without cytotoxicdrugs on pemphigus intercellular antibodies. J Am Acad Dermatol, 2011, 64(3), 484–9.
[1083] Feldmeyer, L; Benden, C; Haile, S; et al. Not all intravenous immunoglobulin preparations are equally well tolerated. Acta Derm Venereol, 2010, 90(5), 494–7.
[1084] Ballow, M. Immunoglobulin therapy: methods of delivery. J Allergy Clin Immunol, 2008, 122(5), 1038–9.
[1085] Carr, DR; Heffernan, MP. Innovative uses of rituximab in dermatology. Dermatol Clin, 2010, 28(3), 547–57.
[1086] Joly, P; Mouquet, H; Roujeau, JC; et al. A single cycle of rituximab for the treatment of severe pemphigus. N Engl J Med, 2007, 357(6), 545–52.
[1087] Sanz, I. Indications of rituximab in autoimmune diseases. Drug Discov Today Ther Strateg, 2009, 6(1), 13–9.
[1088] Maloney, DG. Phase I clinical trial using escalating single-dose infusion of chimeric anti-CD20 monoclonal antibody (IDEC-C2B8) in patients with recurrent B-cell lymphoma. Blood, 1994, 84(8), 2457–66.
[1089] Edwards, JC; Cambridge, G. B-cell targeting in rheumatoid arthritis and other autoimmune diseases. Nat Rev Immunol, 2006, 6(5), 394–403.
[1090] Schmidt, E. Rituximab in refractory autoimmune bullous diseases. Clin Exp Dermatol, 2006, 31(4), 503–8.
[1091] McDonald, V; Leandro, M. Rituximab in non haematological disorders of adults and its mode of action. Br J Haematol, 2009, 146(3), 233–46.
[1092] Onrust, SV; Lamb, HM; Balfour, JA. Rituximab. Drugs, 1999, 58(1), 79–88, discussion 89–90.
[1093] Horvath, B. Low-dose rituximab is effective in pemphigus. Br J Dermatol, 2012, 166(2), 405–12.
[1094] Winkler, U; Jensen, M; Manzke, O; Schulz, H; Diehl, V; Engert, A. Cytokine-release syndrome in patients with B-cell chronic lymphocytic leukemia and high lymphocyte counts after treatment with an anti-CD20 monoclonal antibody (rituximab, IDEC-C2B8). Blood, 1999, 94, 2217-24.
[1095] Arin, MJ; Hunzelmann, N. Anti-B-cell-directed immunotherapy (rituximab) in the treatment of refractory pemphigus-an update. Eur J Dermatol, 2005, 15, 224-30.
[1096] Lowndes, S; Darby, A; Mead, G; Lister, A. Stevens-Johnson syndrome after treatment with rituximab. Ann Oncol, 2002, 13, 1948-50.
[1097] Yang, H; Rosove, MH; Figlin, RA. Tumor lysis syndrome occurring after the administration of rituximab in lymphoproliferative disorders: high-grade non-Hodgkins lymphoma and chronic lymphocytic leukaemia. Ann J Haematol, 1999, 62, 247-50.
[1098] Bermudez, A; Marco, F; Conde, E; Mazo, E; Recio, M; Zubizaretta, A. Fatal varicella-zoster infection following rituximab and chemotherapy treatment in a patient with follicular lymphoma. Haematologica, 2000, 85, 894-5.
[1099] Quartier, P; Tournilhac, O; Archimbaud, C; et al. Enteroviral meningoencephalitis after anti-CD20 (rituximab) treatment. Clin Infect Dis, 2003, 36, 47-9.
[1100] Jourdan, E; Topart, D; Richard, B; Jourdan, J; Sotto, A. Severe autoimmune hemolytic anemia following rituximab therapy in a patient with a lymphoproliferative disorder. Leuk Lymphoma, 2003, 44, 889-90.
[1101] Qazilbash, MH; Qu, Z; Hosing, C; et al. Rituximab-induced acute liver failure after an allogeneic transplantation for chronic myeloid leukemia. Am J Hematol, 2005, 80, 43-5.
[1102] Clifford, KS; Demierre, MF. Progression of classic Kaposi’s sarcoma with rituximab. J Am Acad Dermatol, 2005, 53, 155-7.
[1103] Dunleavy, K; Hakim, F; Kim, HK; Janik, JE; Grant, N; Nakayama, T; et al. B-cell recovery following rituximab-based therapy is associated with perturbations in stromal derived factor-1 and granulocyte homeostasis. Blood, 2005, 106, 795-802.
[1104] Le Roux-Villet, C; et al. Rituximab for patients withrefractory mucous membrane pemphigoid. ArchDermatol., 2011, 147, 843–9.
[1105] Mercader, P. Fatal Pseudomona pneumonia followingrituximab therapy in a patient with epidermolysisbullosa acquisita. J Eur Acad Dermatol Venereol, 2007, 21(8), 1141–2.
[1106] Rios-Fernandez, R. Late-onset neutropenia following rituximab treatment in patients with autoimmune diseases. Br J Dermatol, 2007, 157(6), 1271–3.
[1107] Li, WW. Haemolytic anaemia following rituximab treatment in a patient with pemphigus vulgaris. Br J Dermatol, 2009, 161(1), 205–6.
[1108] Smith, MR. Rituximab (monoclonal anti-CD20 antibody): mechanism of action and resistance. Oncogene, 2003, 22, 7359-68.
[1109] Maloney, DG; Smith, B; Rose, A. Rituximab: mechanism of actionand resistance. Semin Oncol, 2002, 29(Suppl 2), 2-9.
[1110] Matsukura, S. Effect of a single-cycle alternative dosing regimen for rituximab for recalcitrant pemphigus: a case series of 9 patients. Arch Dermatol, 2012, 148(6), 734–9.
[1111] Diab, M. Treatment of refractory pemphigus erythematosus with rituximab. Int J Dermatol, 2008, 47(12), 1317–8.
[1112] Fernando, SL; O’Connor, KS. Treatment of severe pemphigus foliaceus with rituximab. Med J Aust, 2008, 189(5), 289–90.
[1113] Serrao, VV. Successful treatment of recalcitrant pemphigus foliaceus with rituximab. J Eur Acad Dermatol Venereol, 2008, 22(6), 768–70.
[1114] Sorce, M; Arico, M; Bongiorno, MR. Rituximab in refractory pemphigus vulgaris. Dermatol Ther, 2008, 21 Suppl 1, S6–9.
[1115] Goh, MS. Rituximab in the adjuvant treatment of pemphigus vulgaris: a prospective open-label pilot study in five patients. Br J Dermatol, 2007, 156(5), 990–6.
[1116] Marzano, AV. Treatment of refractory pemphigus with the anti-CD20 monoclonal antibody (rituximab). Dermatology, 2007, 214(4), 310–8.
[1117] Arin, MJ. Anti-CD20 monoclonal antibody (rituximab) in the treatment of pemphigus. Br J Dermatol, 2005, 153(3), 620–5.
[1118] Cooper, HL. Treatment of resistant pemphigus vulgaris with an anti-CD20 monoclonal antibody (Rituximab). Clin Exp Dermatol, 2003, 28(4), 366–8.
[1119] Virgolini, L; Marzocchi, V. Anti-CD20 monoclonal antibody (rituximab) in the treatment of autoimmune diseases. Successful result in refractory Pemphigus vulgaris: report of a case. Haematologica, 2003, 88(7), ELT24.
[1120] Fuertes, I. Rituximab in childhood pemphigus vulgaris: a long-term follow-up case and review of the literature. Dermatology, 2010, 221(1), 13–6.
[1121] Connelly, EA. Generalized erythrodermic pemphigus foliaceus in a child and its successful response to rituximab treatment. Pediatr Dermatol, 2007, 24(2), 172–6.
[1122] Kong, HH. Successful treatment of refractory childhood pemphigus vulgaris with anti-CD20 monoclonal antibody (rituximab). Pediatr Dermatol, 2005, 22(5), 461–4.
[1123] Schmidt, E. Long-standing remission of recalcitrantjuvenile pemphigus vulgaris after adjuvant therapywith rituximab. Br J Dermatol, 2005, 153(2), 449–51.
[1124] Ahmed, A. Use of intravenous immunoglobulin therapy in autoimmune blistering diseases. IntImmunopharmacol, 2006, 6, 557–78.
[1125] Cianchini, G. Treatment of severe pemphiguswith rituximab: report of 12 cases and a review of theliterature. Arch Dermatol, 2007, 143(8), 1033–8.
[1126] Cianchini, G. Therapy with rituximab for autoimmunepemphigus: results from a single-centerobservational study on 42 cases with long-term follow-up. J Am Acad Dermatol, 2012, 67(4), 617–22.
[1127] Kim, JH. Clinical efficacy of different doses of rituximab in the treatment of pemphigus: a retrospective study of 27 patients. Br J Dermatol, 2011, 165(3), 646–51.
[1128] Lunardon, L. Adjuvant rituximab therapy of pemphigus: a single-center experience with 31 patients. Arch Dermatol, 2012, 148(9), 1031–6.
[1129] Weger, W; Aberer, E. Treatment failure with rituximab in a patient with pemphigus vulgaris. J Eur Acad Dermatol Venereol, 2008, 22(3), 387–9.
[1130] Karampetsou, MP; Liossis, SNC; Sfikakis, PP. TNFα antagonists beyond approved indications: stories of success and prospects for the future. Q J Med, 2010, 103, 917-28.
[1131] Bachmann, F; Nast, A; Sterry, W; Phillips, S. Safety and efficacy of the tumor necrosis factor antagonists. Semin Cutan Med Surg, 2010, 29, 35-47.
[1132] Guhl, G; Diaz-Ley, B; Fernandez-Herrera, J. Off-label use of biologic agents in the treatment of dermatosis, Part 2: Etanercept, Efalizumab, Alefacept, Rituximab, Daclizumab, Basiliximab, Omalizumab y Cetuximab. Actas Dermosifiliogr, 2008, 99, 5-33.
[1133] Fiorentino, DF; García, MS; Rehmus, W; BoerKimball, AB. A pilot study of etanercept treatment for pemphigus vulgaris. Arch Dermatol, 2011, 147 (1), 117-8.
[1134] Lin, MH; Hsu, CK; Lee, JY. Successful treatment of recalcitrant pemphigus vulgaris and pemphigus vegetans with etanercept and carbon dioxide laser. Arch Dermatol, 2005, 141, 680-2.
[1135] Ikumi, N; Matsukawa, Y; Kuwana, Y; et al. Staphylococcus aureus sepsis after etanercept induction in a hemodialysis patient. Hemodial Int, 2013, 17(1), 133-5.
[1136] Díaz-Lagares, C; Pérez-Alvarez, R; García-Hernández, FJ; et al. Rates of, and risk factors for, severe infections in patients with systemic autoinmune diseases receiving biological agents off-label. Arthritis Res Ther, 2011, 13, R1-12.
[1137] Daulat, S; Detweiler, JG; Pandya, AG. Development of pemphigus vulgaris in a patient with psoriasis treated with etanercept. JEADV, 2009, 23, 441-6.
[1138] Tirado-Sánchez, A; Bonifaz, A; Montes de Oca-Sánchez, G; Ponce-Olivera, RM. Etanercept plus methotrexate: An effective combination therapy for recalcitrant pemphigus. J Res Med Sci, 2015, 20, 317.
[1139] Hall, R; Fairley, J; Woodley, D; Werth, V. Treatment of pemphigus vulgaris patients with infliximab and prednisone is associated with decreased autoantibodies and an increase in immature B cells. J Investig Dermatol, 2012, 132, S89.
[1140] Hall, RP; 3rd; Fairley, J; Woodley, D; et al. A multicentre randomized trial of the treatment of patients with pemphigus vulgaris with infliximab and prednisone compared with prednisone alone. Br J Dermatol, 2015, 172(3), 760-8.
[1141] Anolik, JH; Ravikumar, R; Barnard, J et al. Cutting edge: anti-tumor necrosis factor therapy in rheumatoid arthritis inhibits memory B lymphocytes via effects on lymphoid germinal centers and follicular dendritic cell networks. J Immunol, 2008, 180, 688–92.
[1142] El-Darouti, M; Marzouk, S; Abdel Hay, R; et al. The use of sulfasalazine and pentoxifylline (low cost antitumour necrosis factor drugs) as adjuvant therapy for thetreatment of pemphigus vulgaris: a comparative study. Br JDermatol, 2009, 161(2), 313–9.
[1143] Rashid, RM; Ibrahim, S; Patel, V. Painful pemphigus vulgaris. Anesth Analg, 2007, 104, 233.
[1144] Iraji, F; Yoosefi, A. Healing effect of pilocarpine gel 4% on skin lesions of pemphigus vulgaris. Int J Dermatol, 2006, 45, 743–746.
[1145] Bystryn, JC; Rudolph, JL. Pemphigus. Lancet, 2005, 366, 61–73.
[1146] Vun, YY; Lun, K; Strutton, G. Use of biosynthetic dressings in paraneoplastic pemphigus. Australas J Dermatol, 2004, 45, 133–135.
[1147] Epstein, JB; Gorsky, M; Epstein, MS; et al. Topical azathioprine in the treatment of immune-mediated chronic oral inflammatory conditions: a series of cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2001, 91, 56–61.
[1148] Lozada-Nur, F; Miranda, C; Maliksi, R. Double-blind clinical trial of 0.05% clobetasol propionate (corrected from propionate) ointment in Orabase and 0.05% fluocinonide ointment in Orabase in the treatment of patients with oral vesiculoerosive diseases. Oral Surg Oral Med Oral Pathol, 1994, 77, 598–604.
[1149] Gach, JE; Ilchyshyn, A. Beneficial effects of topical tacrolimus on recalcitrant erosions of pemphigus vulgaris. Clin Exp Dermatol, 2004, 29, 271–272.
[1150] Martin, L; Murrell, D. Measuring the immeasurable: a systematic review of outcome measures in pemphigus. Australas J Dermatol, 2006, 47(Suppl1), A32–3.
[1151] Sebaratnam, D; Murrell, D. Objective scoring systemsfor disease activity in autoimmune bullous disease. Dermatol Clin, 2011, 29(3), 515–20.
[1152] Pfutze, M; Niedermeier, A; Hertl, M; et al. Introducinga novel Autoimmune Bullous Skin Disorder IntensityScore (ABSIS) in pemphigus. Eur J Dermatol, 2007, 17(1), 4–11.
[1153] Saraswat, A; Kumar, B. A new grading system for oralpemphigus. Int J Dermatol, 2003, 42(5), 413–4.
[1154] Pfütze, M; Eming, R; Kneisel, A; et al. Clinical andimmunological follow-up of pemphigus patients onadjuvant treatment with immunoadsorption or rituximab. Dermatology, 2009, 218, 237–45.
[1155] Zhong, S; Qiu, YF; Han, BB; et al. Detection of serumdesmoglein antibody level using enzyme-linkedimmunosorbent assay (ELISA) for monitoring diseaseactivity in patients with pemphigus vulgaris. Beijing Da Xue Xue Bao, 2011, 43, 414–5.
[1156] Souza, SR; Azulay-Abulafia, L; Nascimento, LV. Validation of the commitment index of skin andmucous membranes in pemphigus vulgaris for the clinical evaluation of patients with pemphigus vulgaris. An Bras Dermatol, 2011, 86(2), 284–91.
[1157] Agarwal, M; Walia, R; Kochhar, AM; et al. Pemphigus Area and Activity Score (PAAS)—a novel clinical scoring method for monitoring of pemphigus vulgaris patient. Int J Dermatol, 1998, 37(2), 158–9.
[1158] Herbst, A; Bystryn, JC. Patterns of remission in pemphigus vulgaris. J Am Acad Dermatol, 2000, 42(3), 422–7.
[1159] Mahanjan, VK; Sharma, NL; Sharma, RC; et al. Twelveyearclinico-therapeutic experience in pemphigus, aretrospective study of 54 cases. Int J Dermatol, 2005, 44(10), 821–7.
[1160] Harman, KE; Seed, PT; Gratian, MJ; et al. The severity of cutaneous and oral pemphigus is related to desmoglein1 and 3 antibody levels. Br J Dermatol, 2001, 144(4), 775–80.
[1161] Dakkak, M; Bennet, JR. A new dysphagia score withobjective validation. J Clin Gastroenterol, 1992, 14(2), 99–100.
[1162] Sebaratnam, D; Venugopal, S; Murrell, D. The development of an excel program to compare disease-specific instruments for assessing activity and the extent of autoimmune bullous disease. Australas J Dermatol, 2009, 50(Suppl2), A48.
[1163] Rapp, S; Feldman, S; Exum, M; et al. Psoriasis causes as much disability as other major medical diseases. J Am Acad Dermatol, 1999, 41, 401–7.
[1164] Sheffield, D; Biles, PL; Orom, H; Maixner, W; Sheps DS. Race and sex differences in cutaneous pain perception. Psychosom Med, 2000, 62, 517–23.
[1165] Ryan, TJ. Disability in dermatology. Br J Hosp Med, 1991, 46, 33–6.
[1166] Tabolli, S; Alessandroni, L; Gaido, J; Sampogna, F; Di Pietro, C; Abeni, D. Health-related quality of lifeand nail disorders. Acta Derm Venereol, 2007, 87, 255–9.
[1167] De Korte, J; Mombers, FM; Sprangers, MA; Bos, JD. The suitability of quality of life questionnaires for psoriasis research: a systematic literature review. Arch Dermatol, 2002, 138, 1221–7.
[1168] Ferrario, SR; Baiardi, P; Zotti, AM. Update on family strain questionnaire: a tool for the general screening of caregiving-related problems. Qual Life Res, 2004, 13, 1425–34.
[1169] Sampogna, F; Tabolli, S; Soderfeldt, B; et al. Measuring quality of life of patients with different clinical types of psoriasis using the SF-36. Br J Dermatol, 2006, 154, 844–9.
[1170] Masahiro, S; Shigaku, I; Yutaka, I; et al. An investigation of quality of life (QOL) of pemphigus patients in Japan (first report). J Dermatol, 2000, 110, 283–8.
[1171] Terrab, Z; Benchikhi, H; Maaroufi, A; et al. Quality of life and pemphigus. Ann Dermatol Venereol, 2005, 132, 321–8.
[1172] Mayrshofer, F; Hertl, M; Stinkraven, R; et al. Significant decrease in quality of life in patients with pemphigus vulgaris: results from the German bullous skin disease (BSD) study group. J Dtsch Dermatol Ges, 2005, 3, 431–5.
[1173] Kirtschig, G; Middleton, P; Bennett, C; et al. Interventions for bullous pemphigoid. Cochrane Database Syst Rev, 2010, (10), CD002292.
[1174] Sampogna, F; Picardi, A; Melchi, C; et al. The impact of skin diseases on patients: comparing dermatologist’s opinions with research data collected on patients. Br J Dermatol, 2003, 148, 989–95.
[1175] Sampogna, F; Picardi, A; Chren, MM; et al. Association betweenpoorer quality of life and psychiatric morbidity inpatients with different dermatological conditions. Psychosom Med, 2004, 66, 620–4.
[1176] Tabolli, S; Mozzetta, A; Antinone, V; Alfani, S; Cianchini, G; Abeni, D. The health impact of pemphigus vulgaris and pemphigus foliaceus assessed usingthe medical outcomes study 36-item short form health survey questionnaire. Br J Dermatol, 2008, 158, 1029–34.
[1177] Paradisi, A; Sampogna, F; Di Pietro, C; et al. Quality of life assessment in patients with pemphigus using a minimum set of evaluation tools. J Am Acad Dermatol, 2009, 60(2), 261–9.
[1178] Apolone, G; Mosconi, P. The Italian SF-36 health survey: translation, validation and norming. J Clin Epidemiol, 1998, 51, 1025–36.
[1179] Darjani, A; Ghanbari, A; Sayadi Nejhad, A. Comparison of the health-related quality of life of patients suffering from pemphigus with healthy people. J Guilan Univ Med Sci, 2008, 17, 1–9.
[1180] Timóteo, P; Simões Marques, L; Bertoncello, D. Physiotherapy intervention promotes better quality of life for patients with pemphigus. Rev Soc Bras Med Trop, 2010, 43, 580–3.
[1181] Ghodsi, SZ; Chams-Davatchi, C; Daneshpazooh, M; et al. Quality of life and psychological status of patients with pemphigus vulgaris using DLQI and general health questionnaires. J Dermatol, 2012, 39(2), 141–4.
[1182] Tabolli, S; Pagliarello, C; Paradisi, A; et al. Burden of disease during quiescent periods in patients with pemphigus. Br J Dermatol, 2014, 170(5), 1087–91.
[1183] Tabolli, S; Sampogna, F; Di Pietro, C; et al. Quality of life in patients with epidermolysis bullosa. Br J Dermatol, 2009, 161, 869–77.
[1184] Paradisi, A; Cianchini, G; Lupi, F; et al. QoL in patients with pemphigus receiving adjuvant therapy. Clin Exp Dermatol, 2012, 37(6), 626–30.
[1185] Hanna, A; Sebaratnam, D; Chee, S; et al. A disease-specific quality of life instrument for autoimmune bullous diseases—the ABQOL. Aust J Dermatol, 2010, 52 Suppl 1, 27.
[1186] Sebaratnam, D; Chee, SN; Venugopal, S; et al. Advances in the clinical assessment of autoimmune bullous disease: the development of a disease-specific qualityof life instrument—the ABQOL. J Invest Dermatol, 2009, 129, 2908–23.
[1187] Sebaratnam, DF; McMillan, JR; Werth, VP; et al. Quality of life in patients with bullous dermatoses. Clin Dermatol, 2012, 30, 103–7.
[1188] Sampogna, F; Chren, MM; Melchi, CF; Pasquini, P;Tabolli, S; Abeni, D. Age, gender, quality of life and psychological distress in patients hospitalized with psoriasis. Br J Dermatol, 2006, 154, 325–31.
[1189] Sampogna, F; Sera, F; Abeni, D. IDI Multipurpose Psoriasis Research on Vital Experiences (IMPROVE) investigators. Measures of clinical severity, quality of life, and psychological distress in patients with psoriasis: a cluster analysis. J Invest Dermatol, 2004, 122, 602–7.
[1190] Kiebzak, G; Pierson, L; Campbell, M; et al. Use of the SF36 general health status survey to document health related quality of life in patients with coronary artery disease: effect of disease and response to coronary artery bypass graft surgery. Heart Lung, 2002, 31(3), 207–13.
[1191] Wiebe, S; Guyatt, G; Weaver, B; et al. Comparative responsiveness of generic and specific quality-of-life instruments. J Clin Epidemiol, 2003, 56, 52–60.
[1192] Ware Jr, J; Sherbourne, C. The MOS 36-item short form health survey (SF-36). Conceptual framework and item selection. Med Care, 1992, 30, 472–83.
[1193] Anderson, RT; Rajagopalan, R. Development and validation of a quality of life instrument for cutaneous disease. J Am Acad Dermatol, 1997, 37, 41–50.
[1194] Finlay, A; Khan, G. Dermatology Life Quality Index (DLQI)—a simple practical measure for routine clinical use. Clin Exp Dermatol, 1994, 19, 210–6.
[1195] Morgan, M; McCreedy, R; Simpson, J; Hay, RJ. Dermatology quality of life scales: a measure of impact of skin diseases. Br J Dermatol, 1997, 136, 202–6.
[1196] Chren, MM; Lasek, RJ; Flacke, SA; Zyzanski, SJ. Improved discriminative and evaluative capability of a refined version of Skindex, a quality of life instrument for patients with skin diseases. Arch Dermatol, 1997, 133, 1433–40.
[1197] Chren, MM; Lasek, RJ; Sahay, AP; Sands, LP. Measurement properties of Skindex-16: a brief quality-of-life measure for patients with skin disease. J Cutan Med Surg, 2001, 5, 105–10.
[1198] Nijsten, T; Sampogna, F; Chren, M; et al. Testing and reducing Skindex-29 using Rasch analysis: skindex-17. J Invest Dermatol, 2006, 126, 1244–50.
[1199] Abeni, D; Picardi, A; Pasquini, P; et al. Further evidence of the validity and reliability of the Skindex-29: an Italian study on 2, 242 dermatological outpatients. Dermatology, 2002, 204, 43–9.
[1200] Cohen, A; Ofek-Schlomai, A; Vardy, D; et al. Depression in dermatological patients identified by the mini international neuropsychiatric interview questionnaire. J Am Acad Dermatol, 2005, 54(1), 94–9.
[1201] Goldberg, D; Williams, P. A user’s guide to the general health questionnaire. Windsor: NFER-Nelson, 1998.
[1202] Goldberg, D. The detection of psychiatric illness by questionnaire. London: Oxford University Press, 1972.
[1203] Picardi, A; Abeni, D; Pasquini, P. Assessing psychological distress in patients with skin diseases: reliability, validity and factor structure of the GHQ-12. J Eur Acad Dermatol Venereol, 2001, 15, 410–7.
[1204] Renzi, C; Tabolli, S; Picardi, A; et al. Effects of patient satisfaction with care on health-related quality of life: a prospective study. J Eur Acad Dermatol Venereol, 2005, 19, 712–8.
[1205] Chee, S; Martin, L; Murrell, D. The development of a quality of life instrument specific for pemphigus. J Invest Dermatol, 2009, 129, 2908–23.
[1206] Chen, S. Dermatology quality of life instruments: sorting out the quagmire. J Invest Dermatol, 2007, 127, 2726–39.
[1207] Frew, JW; Murrell, DF. Quality of life measurements inepidermolysis bullosa: tools for clinical research andpatient care. Dermatol Clin, 2010, 28, 185–90.
[1208] Frew, JW; Venugopal, SS; Murrell, DF. Quality of life outcomes of cultured allogeneic fibroblast therapy recipients with epidermolysis bullosa. Aust J Dermatol, 2011, 52 Suppl 1, 26.
[1209] Both, H; Essink-Bot, M; Busschbach, J; et al. Critical review of generic and dermatology-specific health related quality of life instruments. J Invest Dermatol, 2007, 127, 2726–39.
[1210] Horn, HM; Tidman, MJ. Quality of life in epidermolysis bullosa. Clin Exp Dermatol, 2002, 27, 707–10.
[1211] Maroti, M; Ulff, E; Wijma, B. Quality of life before and 6 weeks after treatment in a dermatological outpatient treatment unit. J Eur Acad Dermatol Venereol, 2006, 20(9), 1081–5.
[1212] VanBeek, M; Beach, S; Braslow, L; et al. Highlights from the report of the working group on “Core measures of the burden of skin diseases.” J Invest Dermatol, 2007, 127, 2701–6.
[1213] Sampogna, F; Tabolli, S; Abeni, D. Impact of different skin conditions on quality of life. G Ital Dermatol Venereol, 2013, 148(3), 255-61.
[1214] Timóteo, RP; Marques, LS; Bertoncello, D. Physiotherapy intervention promotes better quality of life for individuals with pemphigus. Rev Soc Bras Med Trop, 2010, 43(5), 580-3.
[1215] Ghodsi, SZ; Chams-Davatchi, C; Daneshpazhooh, M; Valikhani, M; Esmaili, N. Quality of life and psychological status of patients with pemphigus vulgaris using Dermatology Life Quality Index and General Health Questionnaires. J Dermatol, 2012, 39(2), 141-4.
[1216] Rajan, B; Ahmed, J; Shenoy, N; Denny, C; Ongole, R; Binnal, A. Assessment of quality of life in patients with chronic oral mucosal diseases: a questionnaire-based study. Perm J, 2014, 18(1), e123-7.

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