Toll样受体参与类风湿性关节炎发病机制的研究进展  

Advances in research on Toll-like receptors involved in the pathogenesis of rheumatoid arthritis

作　　者：吕社民[1] 孟列素[1] 朱文华[1] 

机构地区：[1]西安交通大学医学部基础医学院生物化学与分子生物学系,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2014年第4期423-428,共6页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.81273211;81302527);中国博士后科学基金资助项目(2013M542356);陕西省国际合作重点项目(2013KW21)~~

摘　　要：类风湿性关节炎(rheumatoid arthritis,RA)作为一种自身免疫性疾病,其病情迁延,是造成我国人群劳动力丧失与致残的主要病因之一。因此,对其病因和发病机制的阐明就显得尤为重要。近年来,Toll样受体(toll-like receptors,TLRs)在RA和实验性关节炎中的作用机制受到了广泛关注。已经发现RA患者的滑膜组织(细胞)、免疫细胞等都存在某些TLR表达的改变。这些TLR可介导滑膜成纤维细胞的细胞因子、趋化因子、基质金属蛋白酶等的产生,同时参与巨噬细胞、树突状细胞、T细胞、B细胞等免疫细胞的功能调节,也能通过对血管内皮细胞及软骨细胞的功能调节,促进血管生成和软骨破坏,从而参与RA及实验性关节炎的进展。总之,多种TLR在不同细胞中协同或拮抗发挥作用,共同参与并影响了关节炎的发病过程,相关的研究为RA的早期预防、诊断、治疗及特异性药物的开发提供了实验依据。Rheumatoid arthritis （RA）,an autoimmune disorder with chronic and protracted course,is perhaps the most severe and disabling type of disease.Therefore,it is vital to clarify the etiology and pathogenesis of RA.Toll-like receptors （TLRs） have been proved to play important roles in pathogenesis of RA and experimental arthritis,thus attracting wide attention in recent years.It has been found that some TLR expressions are dramatically changed in synoviocytes and immune cells of RA patients.The upregulated TLRs can induce the production of cytokines,chemokines and metal matrix proteinases in fibroblast-like synoviocytes,participate in regulating the functions of immune cells such as macrophages,dentritic cells,T cells and B cells,and promote angiogenesis and cartilage destruction by regulating the functions of endothelial cells and chondrocytes.All these contribute to the progression of RA and experimental arthritis.In short,many TLRs of diverse cells exert their actions synergistically or antagonistically to influence the progression of arthritis.Related research will lay significant theoretical foundations for the prevention,diagnosis and therapy of RA and specific drug development.

关 键 词：类风湿性关节炎 TOLL样受体 免疫调节 细胞因子 趋化因子 基质金属蛋白酶 

分 类 号：R593.22[医药卫生—内科学]