白癜风细胞免疫学发病机制的研究进展  

Research Progress on Cellular Immunology Pathogenesis of Vitiligo

作　　者：陈满辉 康晓静 

机构地区：[1]新疆医科大学研究生学院,新疆 乌鲁木齐

出　　处：《临床医学进展》2024年第4期2509-2513,共5页Advances in Clinical Medicine

摘　　要：白癜风是一种获得性免疫介导的色素沉着性疾病,临床特征是皮肤上出现界限清楚的色素脱失。目前的研究结果强调了免疫细胞及其介质在白癜风免疫发病机制中的关键作用。氧化应激介导的先天免疫细胞(如树突状细胞、自然杀伤细胞和ILC-1细胞)的激活被认为是白癜风早期发病的关键事件。先天免疫细胞充当适应性免疫细胞的桥梁,包括T辅助细胞1细胞、细胞毒性T细胞和常驻记忆T细胞。IFN-γ是激活JAK/STAT通路的主要细胞因子介质,导致角质形成细胞产生关键趋化因子CXCL9和CXCL10。免疫细胞和非免疫细胞之间复杂的相互作用最终导致黑素细胞凋亡。本文总结了目前关于导致白癜风的免疫发病机制以及该疾病炎症途径中的关键细胞和细胞因子。Vitiligo is an acquired immune-mediated pigmentation disorder characterized by well-defined depigmentation on the skin. The current research findings emphasize the crucial role of immune cells and their mediators in the immune pathogenesis of vitiligo. The activation of innate immune cells (such as dendritic cells, natural killer cells, and ILC-1 cells) mediated by oxidative stress is considered a key event in the early onset of vitiligo. Congenital immune cells act as a bridge for adaptive immune cells, including T helper cell-1 cells, cytotoxic T cells, and resident memory T cells. IFN-γ is the main cytokine mediator that activates the JAK/STAT pathway, leading to the production of key chemokines CXCL9 and CXCL10 by keratinocytes. The complex interactions between immune cells and non immune cells ultimately lead to melanocyte apoptosis. This article summarizes the current immune pathogenesis of vitiligo and the key cells and cytokines involved in the inflammatory pathway of the disease.

关 键 词：白癜风 细胞因子 自身免疫 

分 类 号：R75[医药卫生—皮肤病学与性病学]