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

作　　者：黄明艳 李龙 HUANG Mingyan;LI Long(Guizhou Medical University,Guiyang 550004,China;Department of Rheumatology and Immunology,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,China)

机构地区：[1]贵州医科大学,贵阳550004 [2]贵州医科大学附属医院风湿免疫科,贵阳550004

出　　处：《医学综述》2022年第17期3335-3341,共7页Medical Recapitulate

基　　金：国家自然科学基金(81460254)。

摘　　要：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.

关 键 词：类风湿关节炎 B7家族 自身免疫性疾病 共刺激信号 滑膜炎 

分 类 号：R593.22[医药卫生—内科学]