Department of Medicine, Division of Dermatology, University of Massachusetts Medical School, 364 Plantation St., LRB 325, Worcester, MA 01605, USA.
Curr Opin Immunol. 2013 Dec;25(6):676-82. doi: 10.1016/j.coi.2013.10.010. Epub 2013 Nov 12.
Vitiligo is an autoimmune disease of the skin in which melanocytes are destroyed by antigen-specific T cells, resulting in patchy depigmentation. Although adaptive immunity plays a clear role in disease progression, initiating factors are largely unknown. Many studies report that cellular stress pathways are dysregulated in melanocytes from vitiligo patients, suggesting that melanocyte-intrinsic defects participate in disease pathogenesis. Recent studies reveal that melanocyte stress generates damage-associated molecular patterns that activate innate immunity, thus connecting stress to organ-specific inflammation. Genetic studies in vitiligo support a role for stress, innate immunity, and adaptive mechanisms. Here, we discuss advances in the field that highlight how cellular stress, endogenous danger signals, and innate immune activation promote the onset of vitiligo.
白癜风是一种皮肤自身免疫性疾病，其中黑素细胞被抗原特异性 T 细胞破坏，导致色素脱失。尽管适应性免疫在疾病进展中起着明显的作用，但启动因素在很大程度上尚不清楚。许多研究报告称，白癜风患者的黑素细胞中细胞应激途径失调，表明黑素细胞内在缺陷参与疾病发病机制。最近的研究揭示，黑素细胞应激产生损伤相关分子模式，激活先天免疫，从而将应激与器官特异性炎症联系起来。白癜风的遗传研究支持应激、先天免疫和适应性机制的作用。在这里，我们讨论了该领域的进展，这些进展强调了细胞应激、内源性危险信号和先天免疫激活如何促进白癜风的发生。
