Th17细胞与白癜风的发病机制  

T helper 17 cells in the pathogenesis of vitiligo

作　　者：王翠[1] 许爱娥[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》2014年第3期189-191,共3页International Journal of Dermatology and Venereology

基　　金：国家自然科学基金面上项目（81271758）;浙江省自然科学基金（Z2100973、LYl2H11008）;省部共建项目基金一浙江省医药卫生重大科技计划（WKJ2012-2-036）;杭州市重大科技创新项目（20122513A02）

摘　　要：白癜风是一种常见的皮肤病，其原因是皮肤黑素细胞的缺失。黑素细胞缺失的确切机制尚不清楚，研究指出，细胞免疫在白癜风发病机制中起到重要作用。在某些特定细胞因子的作用下，CD4＋T细胞分化为Th17细胞，Th17细胞可参与多种疾病的发病。在白癜风发病过程中，Thl7细胞和树突细胞数量增多，功能活跃。Th17细胞除主要分泌IL-17外，还分泌IL-6、IL-21、IL-22和肿瘤坏死因子d等细胞因子，他们参与白癜风发病，导致黑素细胞生成减少、萎缩、消失，黑素生成减少，最终形成白癜风。Vitiligo is a common skin disorder due to the loss of cutaneous melanocytes. The exact mechanism underlying melanocyte loss remains unclear, and a large number of observations have pointed to an important role of cellular immunity in vitiligo pathogenesis. Under the action of some specific cytokines, CD4＋ T cells can differentiate into T helper 17 （Thl7） cells that are involved in the pathogenesis of many diseases. The initiation of vitiligo is associated with an increase in the number and activity of Thl7 cells and dendritic cells. Besides interleukin 17 （IL-17）, Thl7 cells secrete IL-6, IL-21, IL-22, tumor necrosis factor-or （TNF- ~）, etc, which may take part in the pathogenesis of vitiligo by inducing decreased generation, shrinkage and disappearance of melanocytes followed by diminished production of melanin.

关 键 词：白癜风 TH17细胞 树突细胞 细胞因子类 

分 类 号：R758.41[医药卫生—皮肤病学与性病学]