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ＲＡ是一类与免疫紊乱等诸因素有关系的炎症性损伤。随着分子生物学研究的深入，发现ＲＡ病变是浸润的白细胞以及血管内皮细胞和滑膜细胞都不同程度地表达Ｐ－，Ｅ－，Ｌ－选择素；ＩＣＡＭ－１，ＬＦＡ－１等免疫球蛋白超家族及ＶＬＡ－１，３４及β＿３亚单位等的整合素。各细胞借助粘附分子的参与而活化，产生多种细胞因子、致炎因子和蛋白水解酶直接或间接地造成ＲＡ滑膜的增生、血管翁形成和骨关节软骨的破坏。随着对粘附分子作用机制认识和理解的加深，以期制定出更为有效的治疗措施。
RA is a type of inflammatory injury that is linked to various factors such as immune disorders. With the deepening of molecular biology research, it was found that infiltrating leucocytes and vascular endothelial cells and synovial cells of RA lesions express P-, E- and L-selectin to varying degrees; immunoglobulin such as ICAM-1 and LFA-1 Protein superfamily and integrins such as VLA-1, 34 and β_3 subunits. Each cell is activated by the participation of adhesion molecules, resulting in a variety of cytokines. Inflammatory factors and proteolytic enzymes directly or indirectly cause RA synovial hyperplasia, vascular Weng formation and destruction of cartilage of the articular cartilage. With the deepening understanding and understanding of the mechanism of adhesion molecules, in order to develop more effective treatment.