Innate immune mechanisms in vitiligo: danger from within.

Innate immune mechanisms in vitiligo: danger from within.
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DOI:
10.1016/j.coi.2013.10.010
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发表时间:
2013-12
影响因子:
7
通讯作者:
Harris JE
Harris JE
中科院分区:
医学2区
文献类型:
--
作者:
Richmond JM;Frisoli ML;Harris JE

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白癜风是一种自身免疫性皮肤疾病,黑素细胞被抗原特异性T细胞破坏,导致斑片状脱色。虽然获得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是未知的。许多研究报道白癜风患者黑素细胞的细胞应激途径调节失调,提示黑素细胞固有缺陷参与了疾病的发病机制。最近的研究表明,黑素细胞应激产生损伤相关的分子模式,激活先天免疫,从而将应激与器官特异性炎症联系起来。白癜风的遗传学研究支持应激、先天免疫和适应机制的作用。在这里,我们讨论该领域的进展,强调细胞应激、内源性危险信号和先天免疫激活如何促进白癜风的发生。
Vitiligo is an autoimmune disease of the skin in which melanocytes are destroyed by antigen-specific T cells, resulting in patchy depigmentation. While 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.
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