References
1. Ezzedine, K., et al., Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res, 2012. 25 (3): p. E1-13.
2. Manga, P., N. Elbuluk, and S.J. Orlow, Recent advances in understanding vitiligo. F1000Res, 2016. 5 : p. 2234.
3. Al Abadie, M.S. and D.J. Gawkrodger, Integrating neuronal involvement into the immune and genetic paradigm of vitiligo. Clin Exp Dermatol, 2020: p. doi: 10.1111/ced.14490.
4. Zhang, Y., et al., The Prevalence of vitiligo: a meta-analysis. Plos One, 2016. 11 (9): p. e0163806.
5. Kent, G. and M. Al’Abadie, Psychologic effects of vitiligo: a critical incident analysis. J Am Acad Dermatol, 1996. 35 (6): p. 895-8.
6. Nogueira, L.S., P.C. Zancanaro, and R.D. Azambuja, Vitiligo and emotions. An Bras Dermatol, 2009. 84 (1): p. 41-5.
7. Kostopoulou, P., et al., Objective vs. subjective factors in the psychological impact of vitiligo: the experience from a French referral centre. Br J Dermatol, 2009. 161 (1): p. 128-33.
8. Parsad, D., S. Dogra, and A.J. Kanwar, Quality of life in patients with vitiligo. Health Qual Life Outcomes, 2003. 1 : p. 58.
9. Porter, J., et al., Personal responses of patients to vitiligo: the importance of the patient-physician interaction. Arch Dermatol, 1978.114 (9): p. 1384-5.
10. Sukan, M. and F. Maner, The problems in sexual functions of vitiligo and chronic urticaria patients. J Sex Marital Ther, 2007.33 (1): p. 55-64.
11. Alikhan, A., et al., Vitiligo: a comprehensive overview Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. J Am Acad Dermatol, 2011. 65 (3): p. 473-91.
12. Parsad, D., et al., Dermatology Life Quality Index score in vitiligo and its impact on the treatment outcome. Br J Dermatol, 2003.148 (2): p. 373-4.
13. Ezzedine, K., et al., Vitiligo. The Lancet, 2015.386 (9988): p. 74-84.
14. Boissy, R.E. and P. Manga, On the etiology of contact/occupational vitiligo. Pigment Cell Res, 2004. 17 (3): p. 208-14.
15. Karagaiah, P., et al., Emerging drugs for the treatment of vitiligo. Expert Opin Emerg Drugs, 2020. 25 (1): p. 7-24.
16. Tobin, D.J., et al., Melanocytes are not absent in lesional skin of long duration vitiligo. J Pathol, 2000. 191 (4): p. 407-16.
17. Ackerman, A.B., H. Kerl, and J. Sánchez, A clinical atlas of 101 common skin diseases : with histopathologic correlation. 2000, New York: Ardor Scribendi.
18. van den Wijngaard, R., et al., Local immune response in skin of generalized vitiligo patients. Destruction of melanocytes is associated with the prominent presence of CLA+ T cells at the perilesional site. Lab Invest, 2000. 80 (8): p. 1299-309.
19. Puri, N., M. Mojamdar, and A. Ramaiah, In vitro growth characteristics of melanocytes obtained from adult normal and vitiligo subjects. J Invest Dermatol, 1987. 88 (4): p. 434-438.
20. Puri, N., M. Mojamdar, and A. Ramaiah, Growth defects of melanocytes in culture from vitiligo subjects are spontaneously corrected in vivo in repigmenting subjects and can be partially corrected by the addition of fibroblast-derived growth factors in vitro. Arch Dermatol Res, 1989.281 (3): p. 178-84.
21. Dell’Anna, M.L., et al., Antioxidants and narrow band-UVB in the treatment of vitiligo: a double-blind placebo controlled trial. Clin Exp Dermatol, 2007. 32 (6): p. 631-6.
22. Schallreuter, K.U., et al., In vivo and in vitro evidence for hydrogen peroxide (H2O2) accumulation in the epidermis of patients with vitiligo and its successful removal by a UVB-activated pseudocatalase. J Investig Dermatol Symp Proc, 1999. 4 (1): p. 91-6.
23. Medrano, E.E. and J.J. Nordlund, Successful culture of adult human melanocytes obtained from normal and vitiligo donors. J Invest Dermatol, 1990. 95 (4): p. 441-5.
24. Dell’Anna, M.L., et al., Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. J Invest Dermatol, 2007.127 (5): p. 1226-33.
25. Shalbaf, M., et al., Presence of epidermal allantoin further supports oxidative stress in vitiligo. Exp Dermatol, 2008.17 (9): p. 761-70.
26. Maresca, V., et al., Increased sensitivity to peroxidative agents as a possible pathogenic factor of melanocyte damage in vitiligo. J Invest Dermatol, 1997. 109 (3): p. 310-3.
27. Jimbow, K., et al., Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase-related protein in vitiligo. Br J Dermatol, 2001. 144 (1): p. 55-65.
28. Gawkrodger, D.J., Pseudocatalase and narrowband ultraviolet B for vitiligo: clearing the picture. Br J Dermatol, 2009. 161 (4): p. 721-2.
29. Spielvogel, R.a.K., GR., Pigmentary disorders of the skin. Lever’s Histopathology of the Skin, 2005(D. E. Elder, R. Elenitsas, B. L. Johansson and G. F. Murphy. Philadelphia, Lippincott Williams & Wilkins:): p. 705-713.
30. Gilhar, A., et al., Vitiligo and idiopathic guttate hypomelanosis. Repigmentation of skin following engraftment onto nude mice. Arch Dermatol, 1989. 125 (10): p. 1363-6.
31. Li, W., S. Wang, and A.-e. Xu, Role of in vivo reflectance confocal microscopy in determining stability in vitiligo: a preliminary study. Indian J Dermatol, 2013. 58 (6): p. 429-32.
32. Rashighi, M. and J.E. Harris, Vitiligo pathogenesis and emerging treatments. Dermatol Clin, 2017. 35 (2): p. 257-65.
33. Sravani, P.V., et al., Determination of oxidative stress in vitiligo by measuring superoxide dismutase and catalase levels in vitiliginous and non-vitiliginous skin. Indian J Dermatol Venereol Leprol, 2009.75 (3): p. 268-71.
34. Schallreuter, K.U., et al., Epidermal H(2)O(2) accumulation alters tetrahydrobiopterin (6BH4) recycling in vitiligo: identification of a general mechanism in regulation of all 6BH4-dependent processes? J Invest Dermatol, 2001. 116 (1): p. 167-74.
35. Xie, H., et al., Vitiligo: how do oxidative stress-induced autoantigens trigger autoimmunity? J Dermatol Sci, 2016. 81 (1): p. 3-9.
36. Wang, Y., S. Li, and C. Li, Perspectives of new advances in the pathogenesis of vitiligo: from oxidative stress to autoimmunity. Medical science monitor : international medical journal of experimental and clinical research, 2019. 25 : p. 1017-1023.
37. Ghanem, G. and J. Fabrice, Tyrosinase related protein 1 (TYRP1/gp75) in human cutaneous melanoma. Mol Oncol, 2011. 5 (2): p. 150-55.
38. James, E.A., M. Pietropaolo, and M.J. Mamula, Immune recognition of β-cells: neoepitopes as key players in the loss of tolerance. Diabetes, 2018. 67 (6): p. 1035-1042.
39. Frisoli, M.L., K. Essien, and J.E. Harris, Vitiligo: mechanisms of pathogenesis and treatment. Annu Rev Immunol, 2020. 38 : p. 621-648.
40. Toosi, S., S.J. Orlow, and P. Manga, Vitiligo-inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8. J Invest Dermatol, 2012. 132 (11): p. 2601-9.
41. Doss, R.W., et al., Heat shock protein-70 expression in vitiligo and its relation to the disease activity. Indian J. Dermatol, 2016.61 (4): p. 408-412.
42. Levandowski, C.B., et al., NLRP1 haplotypes associated with vitiligo and autoimmunity increase interleukin-1beta processing via the NLRP1 inflammasome. Proc Natl Acad Sci U S A, 2013. 110 (8): p. 2952-6.
43. Richmond, J.M., M.L. Frisoli, and J.E. Harris, Innate immune mechanisms in vitiligo: danger from within. Curr Opin Immunol, 2013.25 (6): p. 676-82.
44. Yu, R., et al., Transcriptome analysis reveals markers of aberrantly activated innate immunity in vitiligo lesional and non-lesional skin. PLoS ONE, 2012. 7 (12): p. e51040.
45. Denman, C.J., et al., HSP70i accelerates depigmentation in a mouse model of autoimmune vitiligo. J Invest Dermatol, 2008. 128 (8): p. 2041-8.
46. Mosenson, J.A., et al., Mutant HSP70 reverses autoimmune depigmentation in vitiligo. Sci Transl Med, 2013. 5 (174): p. 174ra28.
47. Zhang, H., et al., Fusion protein of ATPase domain of Hsc70 with TRP2 acting as a tumor vaccine against B16 melanoma. Immunol Lett, 2006.105 (2): p. 167-73.
48. Kroll, T.M., et al., 4-Tertiary butyl phenol exposure sensitizes human melanocytes to dendritic cell-mediated killing: relevance to vitiligo. J Invest Dermatol, 2005. 124 (4): p. 798-806.
49. Mosenson, J.A., et al., Preferential secretion of inducible HSP70 by vitiligo melanocytes under stress. Pigment Cell Melanoma Res, 2014.27 (2): p. 209-20.
50. Sun, L., W. Liu, and L.J. Zhang, The role of Toll-like receptors in skin host defense, psoriasis, and atopic dermatitis. J Immunol Res, 2019. 2019 : p. 1824624.
51. Basak, P.Y., et al., Evaluation of activatory and inhibitory natural killer cell receptors in non-segmental vitiligo: a flow cytometric study. J Eur Acad Dermatol Venereol, 2008. 22 (8): p. 970-6.
52. Henning, S.W., et al., HSP70i(Q435A)-encoding DNA repigments vitiligo lesions in Sinclair swine. J Invest Dermatol, 2018.138 (12): p. 2531-2539.
53. Rodrigues, M., et al., New discoveries in the pathogenesis and classification of vitiligo. J Am Acad Dermatol, 2017. 77 (1): p. 1-13.
54. van den Boorn, J.G., et al., Skin-depigmenting agent monobenzone induces potent T-cell autoimmunity toward pigmented cells by tyrosinase haptenation and melanosome autophagy. J Invest Dermatol, 2011.131 (6): p. 1240-51.
55. Li, S., et al., Activated NLR family pyrin domain containing 3 (NLRP3) inflammasome in keratinocytes promotes cutaneous T-cell response in patients with vitiligo. J Allergy Clin Immunol, 2020.145 (2): p. 632-645.
56. Bauernfeind, F.G., et al., NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression. Journal of immunology (Baltimore, Md. : 1950), 2009. 183 (2): p. 787-791.
57. Zhou, R., et al., A role for mitochondria in NLRP3 inflammasome activation. Nature, 2011. 469 (7329): p. 221-225.
58. Thornberry, N.A., et al., A novel heterodimeric cysteine protease is required for interleukin-1βprocessing in monocytes. Nature, 1992.356 (6372): p. 768-774.
59. Gu, Y., et al., Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme. Science, 1997.275 (5297): p. 206-9.
60. Speeckaert, R. and N. van Geel, Vitiligo: an update on pathophysiology and treatment options. Am J Clin Dermatol, 2017.
61. Badri, A.M., et al., An immunohistological study of cutaneous lymphocytes in vitiligo. J Pathol, 1993. 170 (2): p. 149-55.
62. Wankowicz-Kalinska, A., et al., Immunopolarization of CD4+ and CD8+ T cells to type-1-like is associated with melanocyte loss in human vitiligo. Lab Invest, 2003. 83 (5): p. 683-95.
63. Le Poole, I.C., et al., Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. Am J Pathol, 1996. 148 (4): p. 1219-28.
64. Ogg, G.S., et al., High frequency of skin-homing melanocyte-specific cytotoxic T lymphocytes in autoimmune vitiligo. J Exp Med, 1998.188 (6): p. 1203-8.
65. Strassner, J.P., et al., Suction blistering the lesional skin of vitiligo patients reveals useful biomarkers of disease activity. J Am Acad Dermatol, 2017. 76 (5): p. 847-55.
66. van Geel, N.A., et al., First histopathological and immunophenotypic analysis of early dynamic events in a patient with segmental vitiligo associated with halo nevi. Pigment Cell Melanoma Res, 2010.23 (3): p. 375-84.
67. Palermo, B., et al., Specific cytotoxic T lymphocyte responses against Melan-A/MART1, tyrosinase and gp100 in vitiligo by the use of major histocompatibility complex/peptide tetramers: the role of cellular immunity in the etiopathogenesis of vitiligo. J Invest Dermatol, 2001.117 (2): p. 326-32.
68. van den Boorn, J.G., et al., Autoimmune destruction of skin melanocytes by perilesional T cells from vitiligo patients. J Invest Dermatol, 2009. 129 (9): p. 2220-32.
69. Boniface, K., et al., Vitiligo skin is imprinted with resident memory CD8 T cells expressing CXCR3. J Invest Dermatol, 2018.138 (2): p. 355-64.
70. Grimes, P.E., et al., Topical tacrolimus therapy for vitiligo: therapeutic responses and skin messenger RNA expression of proinflammatory cytokines. J Am Acad Dermatol, 2004. 51 (1): p. 52-61.
71. Rashighi, M., et al., CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo. Sci Transl Med, 2014. 6 (223): p. 223ra23.
72. Bertolotti, A., et al., Type I interferon signature in the initiation of the immune response in vitiligo. Pigment Cell Melanoma Res, 2014. 27 (3): p. 398-407.
73. Wang, X.X., et al., Increased expression of CXCR3 and its ligands in patients with vitiligo and CXCL10 as a potential clinical marker for vitiligo. Br J Dermatol, 2016. 174 (6): p. 1318-26.
74. Harris, J.E., et al., A mouse model of vitiligo with focused epidermal depigmentation requires IFN-gamma for autoreactive CD8(+) T-cell accumulation in the skin. J Invest Dermatol, 2012.132 (7): p. 1869-76.
75. Richmond, J.M., et al., Keratinocyte-derived chemokines orchestrate T-cell positioning in the epidermis during vitiligo and may serve as biomarkers of disease. J Invest Dermatol, 2017. 137 (2): p. 350-358.
76. Harris, J.E., et al., Rapid skin repigmentation on oral ruxolitinib in a patient with coexistent vitiligo and alopecia areata (AA). J Am Acad Dermatol, 2016. 74 (2): p. 370-1.
77. Frisoli, M.L. and J.E. Harris, Vitiligo: mechanistic insights lead to novel treatments. J Allergy Clin Immunol, 2017. 140 (3): p. 654-662.
78. Lahl, K., et al., Selective depletion of Foxp3+ regulatory T cells induces a scurfy-like disease. J Exp Med, 2007. 204 (1): p. 57-63.
79. Eby, J.M., et al., Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation. Pigment Cell Melanoma Res, 2014. 27 (6): p. 1075-85.
80. Gregg, R.K., et al., Mechanisms of spatial and temporal development of autoimmune vitiligo in tyrosinase-specific TCR transgenic mice. Journal of immunology (Baltimore, Md. : 1950), 2010. 184 (4): p. 1909-1917.
81. Chatterjee, S., et al., A quantitative increase in regulatory T cells controls development of vitiligo. J Invest Dermatol, 2014.134 (5): p. 1285-94.
82. Eby, J.M., et al., CCL22 to activate Treg migration and suppress depigmentation in vitiligo. The Journal of investigative dermatology, 2015. 135 (6): p. 1574-1580.
83. Miao, X., et al., PD-L1 reverses depigmentation in Pmel-1 vitiligo mice by increasing the abundance of Tregs in the skin. Scientific Reports, 2018. 8 (1): p. 1605.
84. Lili, Y., et al., Global activation of CD8+ cytotoxic T lymphocytes correlates with an impairment in regulatory T cells in patients with generalized vitiligo. PLoS One, 2012. 7 (5): p. e37513.
85. Klarquist, J., et al., Reduced skin homing by functional Treg in vitiligo. Pigment Cell Melanoma Res, 2010. 23 (2): p. 276-86.
86. Ben Ahmed, M., et al., Functional defects of peripheral regulatory T lymphocytes in patients with progressive vitiligo. Pigment Cell Melanoma Res, 2012. 25 (1): p. 99-109.
87. Terras, S., et al., Immunohistochemical analysis of FOXP3+ regulatory T cells in healthy human skin and autoimmune dermatoses. Int J Dermatol, 2014. 53 (3): p. 294-9.
88. Abdallah, M., et al., Assessment of tissue FoxP3+, CD4+ and CD8+ T-cells in active and stable nonsegmental vitiligo. Int J Dermatol, 2014. 53 (8): p. 940-6.
89. Maeda, Y., et al., Detection of self-reactive CD8⁺ T cells with an anergic phenotype in healthy individuals. Science, 2014.346 (6216): p. 1536-40.
90. Zhen, Y., et al., Enhanced Th1 and Th17 responses in peripheral blood in active non-segmental vitiligo. Arch Dermatol Res, 2016.308 (10): p. 703-710.
91. Wang, C.Q., et al., Th17 cells and activated dendritic cells are increased in vitiligo lesions. PLoS One, 2011. 6 (4): p. e18907.
92. Martins, C., et al., Phenotype and function of circulating memory T cells in human vitiligo. Br J Dermatol, 2020. 183 (5): p. 899-908.
93. Matos, T.R., Is targeting circulating T blood cells a therapeutic option for vitiligo? Br J Dermatol, 2020. 183 (5): p. 803.
94. Cavalié, M., et al., Maintenance therapy of adult vitiligo with 0.1% tacrolimus ointment: a randomized, double blind, placebo-controlled study. J Invest Dermatol, 2015. 135 (4): p. 970-974.
95. Sitek, J.C., M. Loeb, and J.R. Ronnevig, Narrowband UVB therapy for vitiligo: does the repigmentation last? J Eur Acad Dermatol Venereol, 2007. 21 (7): p. 891-6.
96. Mueller, S.N., et al., Memory T cell subsets, migration patterns, and tissue residence. Annual Review of Immunology, 2013. 31 (1): p. 137-161.
97. Steinbach, K., I. Vincenti, and D. Merkler, Resident-memory T cells in tissue-restricted immune responses: for better or worse? Frontiers in immunology, 2018. 9 : p. 2827-2827.
98. Dijkgraaf, F.E., et al., Tissue patrol by resident memory CD8+ T cells in human skin. Nature Immunology, 2019. 20 (6): p. 756-764.
99. Topham, D.J. and E.C. Reilly, Tissue-resident memory CD8+ T cells: from phenotype to function. Frontiers in Immunology, 2018.9 (515).
100. Jiang, X., et al., Skin infection generates non-migratory memory CD8+ T(RM) cells providing global skin immunity. Nature, 2012.483 (7388): p. 227-31.
101. Mackay, L.K., et al., Long-lived epithelial immunity by tissue-resident memory T (TRM) cells in the absence of persisting local antigen presentation. Proc Natl Acad Sci U S A, 2012. 109 (18): p. 7037-42.
102. Seidel, J.A., et al., Skin resident memory CD8(+) T cells are phenotypically and functionally distinct from circulating populations and lack immediate cytotoxic function. Clin Exp Immunol, 2018.194 (1): p. 79-92.
103. McMaster, S.R., et al., Airway-resident memory CD8 T cells provide antigen-specific protection against respiratory virus challenge through rapid IFN-γ production. Journal of immunology (Baltimore, Md. : 1950), 2015. 195 (1): p. 203-209.
104. Malik, B.T., et al., Resident memory T cells in the skin mediate durable immunity to melanoma. Science immunology, 2017. 2 (10): p. eaam6346.
105. Richmond, J.M., et al., Resident memory and recirculating memory T cells cooperate to maintain disease in a mouse model of vitiligo. The Journal of investigative dermatology, 2019. 139 (4): p. 769-778.
106. Richmond, J.M., et al., Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo. Science Translational Medicine, 2018. 10 (450): p. eaam7710.
107. Matos, T.R., et al., Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing αβ T cell clones. The Journal of clinical investigation, 2017. 127 (11): p. 4031-4041.
108. Naughton, G.K., M. Eisinger, and J.C. Bystryn, Antibodies to normal human melanocytes in vitiligo. J Exp Med, 1983. 158 (1): p. 246-51.
109. Naughton, G.K., D. Reggiardo, and J.C. Bystryn, Correlation between vitiligo antibodies and extent of depigmentation in vitiligo. J Am Acad Dermatol, 1986. 15 (5 Pt 1): p. 978-81.
110. Rocha, I.M., et al., Recognition of melanoma cell antigens with antibodies present in sera from patients with vitiligo. Int J Dermatol, 2000. 39 (11): p. 840-3.
111. Farrokhi, S., et al., Assessment of the immune system in 55 Iranian patients with vitiligo. J Eur Acad Dermatol Venereol, 2005.19 (6): p. 706-11.
112. Harning, R., J. Cui, and J.C. Bystryn, Relation between the incidence and level of pigment cell antibodies and disease activity in vitiligo. J Invest Dermatol, 1991. 97 (6): p. 1078-80.
113. Yu, H.S., C.H. Kao, and C.L. Yu, Coexistence and relationship of antikeratinocyte and antimelanocyte antibodies in patients with non-segmental-type vitiligo. J Invest Dermatol, 1993. 100 (6): p. 823-8.
114. Abu Tahir, M., et al., Current remedies for vitiligo. Autoimmun Rev, 2010. 9 (7): p. 516-20.
115. Xie, P., W. Geoghegan, and R. Jordon. Vitiligo autoantibodies. Studies of subclass distribution and complement activation. in J Invest Dermatol. 1991. BLACKWELL PUBLISHING INC 350 MAIN ST, MALDEN, MA 02148 USA.
116. Aronson, P.J. and K. Hashimoto, Association of IgA anti-melanoma antibodies in the sera of vitiligo patients with active disease. J Invest Dermatol, 1987. 88 (475).
117. Zhu, M.C., et al., Detection of serum anti-melanocyte antibodies and identification of related antigens in patients with vitiligo. Genet Mol Res, 2015. 14 (4): p. 16060-73.
118. Cui, J., Y. Arita, and J.C. Bystryn, Characterization of vitiligo antigens. Pigment Cell Res, 1995. 8 (1): p. 53-9.
119. Park, Y.K., et al., Identification of autoantibody to melanocytes and characterization of vitiligo antigen in vitiligo patients. J Dermatol Sci, 1996. 11 (2): p. 111-20.
120. Song, Y.H., et al., The role of tyrosinase in autoimmune vitiligo. Lancet, 1994. 344 (8929): p. 1049-52.
121. Baharav, E., et al., Tyrosinase as an autoantigen in patients with vitiligo. Clin Exp Immunol, 1996. 105 (1): p. 84-8.
122. Kemp, E.H., et al., Detection of tyrosinase autoantibodies in patients with vitiligo using 35S-labeled recombinant human tyrosinase in a radioimmunoassay. J Invest Dermatol, 1997. 109 (1): p. 69-73.
123. Kemp, E.H., et al., Immunoprecipitation of melanogenic enzyme autoantigens with vitiligo sera: evidence for cross-reactive autoantibodies to tyrosinase and tyrosinase-related protein-2 (TRP-2). Clin Exp Immunol, 1997. 109 (3): p. 495-500.
124. Kemp, E.H., et al., Autoantibodies to human melanocyte-specific protein pmel17 in the sera of vitiligo patients: a sensitive and quantitative radioimmunoassay (RIA). Clin Exp Immunol, 1998.114 (3): p. 333-8.
125. Kemp, E.H., et al., Autoantibodies to tyrosinase-related protein-1 detected in the sera of vitiligo patients using a quantitative radiobinding assay. Br J Dermatol, 1998. 139 (5): p. 798-805.
126. Ruiz-Argüelles, A., et al., Treatment of vitiligo with a chimeric monoclonal antibody to CD20: a pilot study. Clin Exp Immunol, 2013.174 (2): p. 229-36.
127. Mandry, R.C., et al., Organ-specific autoantibodies in vitiligo patients and their relatives. Int J Dermatol, 1996. 35 (1): p. 18-21.
128. Kemp, E.H., et al., The melanin-concentrating hormone receptor 1, a novel target of autoantibody responses in vitiligo. J Clin Invest, 2002.109 (7): p. 923-30.
129. Waterman, E.A., et al., Autoantigens in vitiligo identified by the serological selection of a phage-displayed melanocyte cDNA expression library. J Invest Dermatol, 2010. 130 (1): p. 230-40.
130. Faraj, S., et al., An investigation of lamin A autoantibodies in vitiligo. J Invest Dermatol, 2017. 137 (S14).
131. Norris, D.A., et al., Evidence for immunologic mechanisms in human vitiligo: patients’ sera induce damage to human melanocytes in vitro by complement-mediated damage and antibody-dependent cellular cytotoxicity. J Invest Dermatol, 1988. 90 (6): p. 783-9.
132. Gilhar, A., et al., In vivo destruction of melanocytes by the IgG fraction of serum from patients with vitiligo. J Invest Dermatol, 1995.105 (5): p. 683-6.
133. Gottumukkala, R.V., et al., Function-blocking autoantibodies to the melanin-concentrating hormone receptor in vitiligo patients. Lab Invest, 2006. 86 (8): p. 781-9.
134. Yohn, J.J., et al., Cultured human keratinocytes synthesize and secrete endothelin-1. J Invest Dermatol, 1993. 100 (1): p. 23-6.
135. Kemp, E.H., E.A. Waterman, and A.P. Weetman, Autoimmune aspects of vitiligo. Autoimmunity, 2001. 34 (1): p. 65-77.
136. Homey, B., et al., Topical FK506 suppresses cytokine and costimulatory molecule expression in epidermal and local draining lymph node cells during primary skin immune responses. J Immunol, 1998.160 (11): p. 5331-40.
137. Hartmann, A., E.B. Brocker, and H. Hamm, Occlusive treatment enhances efficacy of tacrolimus 0.1% ointment in adult patients with vitiligo: results of a placebo-controlled 12-month prospective study. Acta Derm Venereol, 2008. 88 (5): p. 474-9.
138. Gawkrodger, D.J., et al., Vitiligo: concise evidence based guidelines on diagnosis and management. Postgrad Med J, 2010.86 (1018): p. 466-71.
139. Lee, C.-H., et al., Molecular mechanisms of UV-induced apoptosis and its effects on skin residential cells: the implication in UV-Based phototherapy. Int J Mol Sci, 2013. 14 (3): p. 6414-35.
140. Fishman, P., et al., Vitiligo autoantibodies are effective against melanoma. Cancer, 1993. 72 (8): p. 2365-9.
141. Cario-Andre, M., et al., The melanocytorrhagic hypothesis of vitiligo tested on pigmented, stressed, reconstructed epidermis. Pigment Cell Res, 2007. 20 (5): p. 385-93.
142. Kemp, E.H., E.A. Waterman, and A.P. Weetman, Immunological pathomechanisms in vitiligo. Expert Rev Mol Med, 2001. 3 (20): p. 1-22.
143. Takechi, Y., et al., A melanosomal membrane protein is a cell surface target for melanoma therapy. Clin Cancer Res, 1996.2 (11): p. 1837-42.
144. Leonhardt, R.M., et al., Proprotein convertases process Pmel17 during secretion. J Biol Chem, 2011. 286 (11): p. 9321-37.
145. Martínez-Lostao, L., A. Anel, and J. Pardo, How do cytotoxic lymphocytes kill cancer cells? Clinical Cancer Research, 2015.21 (22): p. 5047.
146. Hassin, D., et al., Cytotoxic T lymphocyte perforin and Fas ligand working in concert even when Fas ligand lytic action is still not detectable. Immunology, 2011. 133 (2): p. 190-196.
147. Spritz, R.A. and G.H. Andersen, Genetics of vitiligo. Dermatol Clin, 2017. 35 (2): p. 245-55.
148. Bethune, M.T. and A.V. Joglekar, Personalized T cell-mediated cancer immunotherapy: progress and challenges. Curr Opin Biotechnol, 2017. 48 : p. 142-152.
149. Leisegang, M., et al., Targeting human melanoma neoantigens by T cell receptor gene therapy. J Clin Invest, 2016. 126 (3): p. 854-8.
150. Singh, M., et al., Cytokines: the yin and yang of vitiligo pathogenesis. Expert Rev Clin Immunol, 2019. 15 (2): p. 177-188.
151. Singh, S., U. Singh, and S.S. Pandey, Serum concentration of IL-6, IL-2, TNF-α, and IFNγ in vitiligo patients. Indian J Dermatol, 2012.57 (1): p. 12-14.
152. Miniati, A., et al., Stimulated human melanocytes express and release interleukin-8, which is inhibited by luteolin: relevance to early vitiligo. Clin Exp Dermatol, 2014. 39 (1): p. 54-57.
153. Gholijani, N., M.R. Yazdani, and L. Dastgheib, Predominant role of innate pro-inflammatory cytokines in vitiligo disease. Arch Dermatol Res, 2020. 312 (2): p. 123-131.
154. Moretti, S., et al., Keratinocyte dysfunction in vitiligo epidermis: cytokine microenvironment and correlation to keratinocyte apoptosis. Histol Histopathol, 2009. 24 (7): p. 849-57.
155. Boukhedouni, N., et al., Type-1 cytokines regulate MMP-9 production and E-cadherin disruption to promote melanocyte loss in vitiligo. JCI Insight, 2020. 5 (11).
156. Lengagne, R., et al., Spontaneous vitiligo in an animal model for human melanoma: role of tumor-specific CD8+ T cells. Cancer Res, 2004.64 (4): p. 1496-501.
157. Garbelli, S., et al., Melanocyte-specific, cytotoxic T cell responses in vitiligo: the effective variant of melanoma immunity? Pigment Cell Res, 2005. 18 (4): p. 234-42.
158. Fishman, P., et al., Autoantibodies to tyrosinase: the bridge between melanoma and vitiligo. Cancer, 1997. 79 (8): p. 1461-4.
159. Huang, S.K., et al., Antibody responses to melanoma/melanocyte autoantigens in melanoma patients. J Invest Dermatol, 1998.111 (4): p. 662-7.
160. Kirkin, A.F., K. Dzhandzhugazyan, and J. Zeuthen, Melanoma-associated antigens recognized by cytotoxic T lymphocytes. Apmis, 1998. 106 (7): p. 665-79.
161. Edwards, J., et al., CD103 + tumor-resident CD8 + T cells are associated with improved survival in immunotherapy-naïve melanoma patients and expand significantly during anti-PD-1 treatment. Clinical Cancer Research, 2018. 24 (13): p. 3036.
162. Teulings, H.-E., et al., Vitiligo-like depigmentation in patients with stage III-IV melanoma receiving immunotherapy and its association with survival: a systematic review and meta-analysis. Journal of Clinical Oncology, 2015. 33 (7): p. 773-781.
163. Yee, C., et al., Melanocyte destruction after antigen-specific immunotherapy of melanoma: direct evidence of T cell–mediated vitiligo. The Journal of experimental medicine, 2000. 192 (11): p. 1637-1644.
164. Tatli, A.M., et al., Association of vitiligo and response in patients with metastatic malignant melanoma on temozolomide. Tumori, 2015. 101 (2): p. e67-9.
165. Alkhateeb, A., et al., Epidemiology of vitiligo and associated autoimmune diseases in Caucasian probands and their families. Pigment Cell Res, 2003. 16 (3): p. 208-14.
166. Picardo, M., et al., Vitiligo. Nat Rev Dis Primers, 2015.1 : p. 15011.
167. Lerner, A.B., Vitiligo. J Invest Dermatol, 1959. 32 (2, Part 2): p. 285-310.
168. Jin, Y., et al., Genome-wide association analyses identify 13 new susceptibility loci for generalized vitiligo. Nat Genet, 2012.44 (6): p. 676-80.
169. Tang, X.F., et al., Association analyses identify three susceptibility Loci for vitiligo in the Chinese Han population. J Invest Dermatol, 2013. 133 (2): p. 403-10.
170. Liu, J.B., et al., Association of vitiligo with HLA-A2: a meta-analysis. J Eur Acad Dermatol Venereol, 2007. 21 (2): p. 205-13.
171. Jin, Y., et al., Variant of TYR and autoimmunity susceptibility loci in generalized vitiligo. N Engl J Med, 2010. 362 (18): p. 1686-97.
172. Jin, Y., et al., Major association of vitiligo with HLA‐A* 02: 01 in Japanese. Pigment Cell Melanoma Res, 2015. 28 (3): p. 360-62.
173. Fain, P.R., et al., HLA class II haplotype DRB1*04-DQB1*0301 contributes to risk of familial generalized vitiligo and early disease onset. Pigment Cell Res, 2006. 19 (1): p. 51-7.
174. Quan, C., et al., Genome-wide association study for vitiligo identifies susceptibility loci at 6q27 and the MHC. Nat Genet, 2010.42 (7): p. 614-8.
175. Tazi-Ahnini, R., et al., The autoimmune regulator gene (AIRE) is strongly associated with vitiligo. Br J Dermatol, 2008. 159 (3): p. 591-6.
176. Oftedal, B.E., et al., Dominant mutations in the autoimmune regulator AIRE are associated with common organ-specific autoimmune diseases. Immunity, 2015. 42 (6): p. 1185-96.
177. Kemp, E.H., et al., Analysis of a microsatellite polymorphism of the cytotoxic T-lymphocyte antigen-4 gene in patients with vitiligo. Br J Dermatol, 1999. 140 (1): p. 73-8.
178. Birlea, S.A., et al., CTLA4 and generalized vitiligo: two genetic association studies and a meta-analysis of published data. Pigment Cell Melanoma Res, 2009. 22 (2): p. 230-4.
179. Pehlivan, S., et al., Association between IL4 (-590), ACE (I)/(D), CCR5 (Delta32), CTLA4 (+49) and IL1-RN (VNTR in intron 2) gene polymorphisms and vitiligo. Eur J Dermatol, 2009. 19 (2): p. 126-8.
180. Li, M., et al., Functional polymorphisms of the FAS gene associated with risk of vitiligo in Chinese populations: a case-control analysis. J Invest Dermatol, 2008. 128 (12): p. 2820-4.
181. Jin, Y., et al., Common variants in FOXP1 are associated with generalized vitiligo. Nat Genet, 2010. 42 (7): p. 576-8.
182. Birlea, S.A., et al., Comprehensive association analysis of candidate genes for generalized vitiligo supports XBP1, FOXP3, and TSLP. J Invest Dermatol, 2011. 131 (2): p. 371-81.
183. Ferrara, T.M., et al., Risk of generalized vitiligo is associated with the common 55R-94A-247H variant haplotype of GZMB (encoding granzyme B). J Invest Dermatol, 2013. 133 (6): p. 1677-9.
184. Jin, Y., et al., Genetic variations in NALP1 are associated with generalized vitiligo in a Romanian population. J Invest Dermatol, 2007.127 (11): p. 2558-62.
185. Jin, Y., et al., NALP1 in vitiligo-associated multiple autoimmune disease. N Engl J Med, 2007. 356 (12): p. 1216-25.
186. Alkhateeb, A. and F. Qarqaz, Genetic association of NALP1 with generalized vitiligo in Jordanian Arabs. Arch Dermatol Res, 2010.302 (8): p. 631-4.
187. Canton, I., et al., A single-nucleotide polymorphism in the gene encoding lymphoid protein tyrosine phosphatase (PTPN22) confers susceptibility to generalised vitiligo. Genes Immun, 2005.6 (7): p. 584-7.
188. LaBerge, G.S., et al., PTPN22 is genetically associated with risk of generalized vitiligo, but CTLA4 is not. J Invest Dermatol, 2008.128 (7): p. 1757-62.
189. Laberge, G.S., et al., The PTPN22-1858C>T (R620W) functional polymorphism is associated with generalized vitiligo in the Romanian population. Pigment Cell Melanoma Res, 2008. 21 (2): p. 206-8.
190. Laddha, N.C., et al., Association of PTPN22 1858C/T polymorphism with vitiligo susceptibility in Gujarat population. J Dermatol Sci, 2008. 49 (3): p. 260-2.
191. Song, G.G., J.H. Kim, and Y.H. Lee, The CTLA-4 +49 A/G, CT60 A/G and PTPN22 1858 C/T polymorphisms and susceptibility to vitiligo: a meta-analysis. Mol Biol Rep, 2013. 40 (4): p. 2985-93.
192. Garcia-Melendez, M.E., et al., Protein tyrosine phosphatase PTPN22 +1858C/T polymorphism is associated with active vitiligo. Exp Ther Med, 2014. 8 (5): p. 1433-37.
193. Ren, Y., et al., Genetic variation of promoter sequence modulates XBP1 expression and genetic risk for vitiligo. PLoS Genet, 2009.5 (6): p. e1000523.
194. Na, G.Y., et al., Polymorphisms in the melanocortin-1 receptor (MC1R) and agouti signaling protein (ASIP) genes in Korean vitiligo patients. Pigment Cell Res, 2003. 16 (4): p. 383-7.
195. Alkhateeb, A., P.R. Fain, and R.A. Spritz, Candidate functional promoter variant in the FOXD3 melanoblast developmental regulator gene in autosomal dominant vitiligo. J Gen Intern Med, 2005. 20 (5): p. 388-91.
196. Jin, Y., et al., Next-generation DNA re-sequencing identifies common variants of TYR and HLA-A that modulate the risk of generalized vitiligo via antigen presentation. J Invest Dermatol, 2012.132 (6): p. 1730-3.
197. Sun, Y., et al., A comprehensive association analysis confirms ZMIZ1 to be a susceptibility gene for vitiligo in Chinese population. J Med Genet, 2014. 51 (5): p. 345-53.
198. Jin, S.Y., et al., Association of angiotensin converting enzyme gene I/D polymorphism of vitiligo in Korean population. Pigment Cell Res, 2004. 17 (1): p. 84-6.
199. Wood, J.M., et al., Computer simulation of heterogeneous single nucleotide polymorphisms in the catalase gene indicates structural changes in the enzyme active site, NADPH-binding and tetramerization domains: a genetic predisposition for an altered catalase in patients with vitiligo? Exp Dermatol, 2008. 17 (4): p. 366-71.
200. Liu, L., et al., Promoter variant in the catalase gene is associated with vitiligo in Chinese people. J Invest Dermatol, 2010.130 (11): p. 2647-53.
201. Mansuri, M.S., et al., The catalase gene promoter and 5’-untranslated region variants lead to altered gene expression and enzyme activity in vitiligo. Br J Dermatol, 2017. 177 (6): p. 1590-1600.
202. Kim, H.J., et al., The association between endothelin-1 gene polymorphisms and susceptibility to vitiligo in a Korean population. Exp Dermatol, 2007. 16 (7): p. 561-6.
203. Gokhale, B.B. and L.N. Mehta, Histopathology of vitiliginous skin. Int J Dermatol, 1983. 22 (8): p. 477-80.
204. Nordlands, J.J., Vitiligo, in In: Pathogenesis of skin diseases, B.H.a.D. Thiers, R. L., Editor. 1986, Churchill Livingstone: New York. p. 99-128.
205. Al’Abadie, M.S., et al., Morphologic observations on the dermal nerves in vitiligo: an ultrastructural study. Int J Dermatol, 1995.34 (12): p. 837-40.
206. Al’Abadie, M., et al., Neuropeptide and neuronal marker studies in vitiligo. Br J Dermatol, 1994. 131 (2): p. 160-65.
207. Dimitrijević, M. and S. Stanojević, The intriguing mission of neuropeptide Y in the immune system. Amino Acids, 2013. 45 (1): p. 41-53.
208. Ganea, D., K.M. Hooper, and W. Kong, The neuropeptide vasoactive intestinal peptide: direct effects on immune cells and involvement in inflammatory and autoimmune diseases. Acta Physiol (Oxf), 2015.213 (2): p. 442-52.
209. Taams, L.S., Neuroimmune interactions: how the nervous and immune systems influence each other. Clin Exp Immunol, 2019. 197 (3): p. 276-277.
210. Kundu, R.V., et al., The convergence theory for vitiligo: a reappraisal. Exp Dermatol, 2019. 28 (6): p. 647-655.
211. Cucchi, M.L., et al., Higher plasma catecholamine and metabolite levels in the early phase of nonsegmental vitiligo. Pigment Cell Res, 2000. 13 (1): p. 28-32.
212. Gauthier, Y., et al., Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo. Br J Dermatol, 2003. 148 (1): p. 95-101.
213. Pichler, R., et al., Vitiligo patients present lower plasma levels of alpha-melanotropin immunoreactivities. Neuropeptides, 2006.40 (3): p. 177-83.
214. Harris, J.E., Chemical-induced vitiligo. Dermatol Clin, 2017.35 (2): p. 151-161.
215. Westerhof, W. and M. d’Ischia, Vitiligo puzzle: the pieces fall in place. Pigment Cell Res, 2007. 20 (5): p. 345-59.
216. Namazi, M.R., Neurogenic dysregulation, oxidative stress, autoimmunity, and melanocytorrhagy in vitiligo: can they be interconnected? Pigment Cell Res, 2007. 20 (5): p. 360-3.