类风湿关节炎病因和发病机制研究进展  

Research Advances in the Etiology and Pathophysiology of Rheumatoid Arthritis

作　　者：魏蕾[1] 姜林娣[1] 

机构地区：[1]复旦大学附属中山医院风湿免疫科,上海200032

出　　处：《医学综述》2015年第9期1548-1551,共4页Medical Recapitulate

摘　　要：类风湿关节炎(RA)是在环境因素、遗传背景以及两者交互作用下,高度异质性的自身免疫性疾病。由于自身免疫耐受被打破,导致免疫细胞和炎性因子活化,自身抗体生成,最终因炎症瀑布放大和慢性炎症造成骨质破坏和关节重构。近年来,研究发现神经免疫调节网络在RA的发病中具有重要作用,是对其发病机制的重要补充。Rheumatoid arthritis is a kind of autoimmune diseases with high heterogeneity, etiology of rheumatoid arthritis is attributed to the environmental factors, gene as well as environmental-genetic interac- tion. Due to the loss of immune tolerance, activated immune cells produce specific autoantibodies and syner- gize with pro-inflammatory cytokines. The amplified inflammation cascade and chronical inflammation lead to the joint destruction and remodeling. In recent years, studies have found that the neuro-immune modulating network plays an important role in the incidence of rheumatoid arthritis and can be a complement of the path- ogenesis of rheumatoid arthritis.

关 键 词：类风湿关节炎 吸烟 人类白细胞抗原-DRB1 关节破坏 神经内分泌网络 

分 类 号：R593.22[医药卫生—内科学]