Th17/Treg失衡在类风湿性关节炎发病机制中的研究  

Research of imbalance of Th17/Treg in the pathogenesis of rheumatoid arthritis

作　　者：章婷婷[1] 骆春艳[1] 王嘉军[1] 

机构地区：[1]三峡大学医学院检验科,湖北宜昌443002

出　　处：《海南医学》2013年第20期3035-3038,共4页Hainan Medical Journal

基　　金：湖北省自然科学基金资助项目(编号:2009CDB280)

摘　　要：类风湿性关节炎(Rheumatoid arthritis,RA)是一种临床常见的自身免疫性疾病,严重影响患者的生活质量。免疫细胞在其发生、发展中发挥重要作用,然而对其具体发病机制目前尚不十分清楚。辅助性T细胞17(Th17)是一类以分泌IL-17为主、可介导RA炎症反应过程的细胞;而调节性T细胞(Treg)则具有免疫抑制作用,Th17/Treg失衡在RA的发病机制中扮演重要角色。本文主要就Th17与Treg的相互作用及Th17/Treg失衡在RA发病机制中的作用做简要综述。Rheumatoid arthritis is a common clinical autoimmune diseases, which seriously affected the quali- ty of life of patients. Immune cells play an important role in the occurrence as well as the development of RA, but its specific pathogenesis is still not clear. T helper 17 cells （Thl 7） mainly secrete IL-17 and can mediate the inflammato- ry response of rheumatoid arthritis, while regulatory T cells suppress the immune response. The imbalance of Thl7/ Treg is of great significance to the pathogenesis of rheumatoid arthritis. This review mainly focuses on the interaction between Thl7 and Treg and the effect ofThl 7/Treg imbalances in the pathogenesis of RA.

关 键 词：类风湿性关节炎 TH17 TREG 发病机制 

分 类 号：R593.22[医药卫生—内科学]