B7家族分子在类风湿关节炎中的研究进展

Research Advances of B7 Family Molecules in Rheumatoid Arthritis

类风湿关节炎(RA)是一种以慢性、进展性、对称性、侵袭性关节炎和滑膜炎为特征的全身性自身免疫性疾病,其发病机制目前尚未完全阐明,可能与T细胞有关。T细胞完全活化需要双重信号刺激,而B7家族分子可为T细胞正常活化提供重要的第二信号,参与维持免疫平衡。B7家族分子异常表达可导致免疫功能失衡、T细胞过度活化并聚集于病变关节,释放大量炎症细胞因子,进而诱发或加重RA。因此,系统整合B7家族中各分子在RA中的作用,可以为进一步探索RA的发病机制提供一定理论依据。

Rheumatoid arthritis(RA)is a systemic autoimmune disease characterized by chronic,progressive,symmetrical and invasive arthritis and synovitis.The pathogenesis of RA has not been fully elucidated,and may be related to T cells.Complete activation of T cells requires dual signals stimulation,and B7 family molecules can provide secondary signals for normal activation of T cells and participate in maintaining immune balance.Abnormal expression of B7 family molecules can lead to immune imbalance,T cells overexpression and aggregation in the diseased joints,and release of a large number of inflammatory cytokines,and then induce or aggravate RA.Therefore,the systematical elaboration on roles of each molecule of B7 family in RA,can provide a theoretical basis for further exploration of the pathogenesis of RA.