白介素-6／gp130信号通路在白癜风T细胞免疫中的作用  

Interleukin-6/gpl30 signaling pathway in vitiligo-associated T cell immunity

作　　者：汤慧娟[1] 许爱娥[2] 周妙妮[2] 

机构地区：[1]安徽医科大学附属杭州临床学院,杭州310009 [2]杭州市第三人民医院皮肤科

出　　处：《国际皮肤性病学杂志》2013年第4期266-269,共4页International Journal of Dermatology and Venereology

基　　金：国家自然科学基金（81071294、81271758）;浙江省自然科学基金（Z2100973）;省部共建项目基金（wKJ2012-2-036）;杭州科技局重大创新项目（20122513A02）

摘　　要：细胞因子通过对T细胞的分化影响适应性免疫应答，IL-6-开始被认为具有B细胞生长因子的特点诱导抗体的产生，最近研究表明，IL-6在T细胞免疫中产生重要的作用，IL-6通过膜结合IL-6受体或可溶性IL-6受体结合gp130形成复合体进行信号转导产生作用，可以阻止T细胞凋亡、诱导Th细胞的活化、调节Treg和，Th17细胞之间的平衡，且T细胞在白癜风中发挥重要作用，黑素细胞自身抗原的存在使自身反应性T细胞可以通过细胞毒性作用持续性杀伤黑素细胞，导致黑素细胞的毁坏和凋亡，从而引起白癜风。Cytokines influence adaptive immune response by determining T cell differentiation. Although interleukin-6 （IL-6） was initially considered to be a B-cell growth factor capable of inducing antibody production, recent studies have shown that it also plays a significant role in T cell differentiation. By binding to membrane-bound form or soluble form of IL-6 receptor （IL-6R） to form a hexameric receptor complex with gpl30 which is capable of inducing signal transduction, IL-6 can inhibit the apoptosis of T ceils, induce the activation of helper T （Th） cells, regulate the balance between regulator T （Treg） and Thl7 ceils. T cells play important roles in the pathogenesis of vitiligo. With the presence of melanocyte autoantigens, autoreactive T ceils can continuously kill melanocytes, cause melanocyte damage and apoptosis, and eventually result in the development of vitiligo.

关 键 词：白癜风 免疫 T淋巴细胞 白细胞介素6 

分 类 号：R758[医药卫生—皮肤病学与性病学]