摘要
类风湿关节炎(rheumatoid arthritis,RA)是一种病因尚未明确的以滑膜慢性炎症为主的自身免疫性疾病,近年研究发现,细胞因子网络失衡在RA的发病和进展中发挥着重要作用,该病的加重或好转依赖于炎性细胞因子和调节性细胞因子之间的动态变化。其中TNF-α、IL-1、IL-17、IL-33等在RA滑膜病变中起核心作用,而IL-4、IL-10、TGF-β等细胞因子却可以起到减轻关节损伤的作用。本文将从致炎细胞因子、抑炎细胞因子与RA之间的关系来阐述RA的发病机制。
Rheumatoid Arthritis (RA) is a kind of selfimmune disease with an unknown pathogen, which mainly manifest- ed the chronic inflammation of synovium. Recent studies have found that the cytokine network plays an important role in the onset and progression of RA, the increase or improve of RA depends on the dynamics between inflammatory cytokines and antiinflammatory cytokines. TNF-α, IL-1, IL-17, IL-33 play a bad role, however, IL-4, IL-10, TGF-β can reduce the joint damage. The progress of study about cytokines on the Rheumatoid Arthritis nosogenesis was described in this re view.
出处
《中国当代医药》
2012年第7期12-14,共3页
China Modern Medicine
基金
贵州省教育厅自然科学研究项目[黔教科(2008032)]
关键词
细胞因子
类风湿关节炎
发病机制
致炎因子
抑炎因子
Cytokines
Rheumatoid arthritis
Nosogenesis
Inflammatory cytokines
Antiinflammatory cytokines