Postigo A A, García-Vicuña R, Laffón A, Sánchez-Madrid F
Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Spain.
Autoimmunity. 1993;16(1):69-76. doi: 10.3109/08916939309010649.
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by infiltration of mononuclear cells, mainly T lymphocytes, into the synovial membrane (SM). The interaction of peripheral blood T cells with the different components of the rheumatoid synovium is mediated by cell surface proteins such as selectins, integrins, members of the immunoglobulin superfamily and homing receptors. T lymphocytes infiltrating the rheumatoid SM show an activated phenotype and display an increased avidity of their adhesion receptors that results in an enhanced interaction of these cells with both extracellular matrix proteins (ECM) and cellular ligands (VCAM-1, ICAMs). The interaction of T cell integrins with their ligands, besides an additional antigenic stimulus, could trigger a mitogenic response on these cells, a phenomenon that can contribute to increased cellularity observed into the rheumatoid SM. Moreover, cell attachment to ECM through integrins induces the secretion of several proteases that can contribute to the tissue damage observed in RA. The increased knowledge about the role of adhesion receptors in the pathogenesis of RA and other inflammatory diseases will allow the introduction of a new therapeutic approach by: the use of specific blocking reagents designed to interfere with the function of adhesion molecules.
类风湿关节炎（RA）是一种慢性炎症性疾病，其特征是单核细胞（主要是T淋巴细胞）浸润滑膜（SM）。外周血T细胞与类风湿滑膜不同成分之间的相互作用是由细胞表面蛋白介导的，如选择素、整合素、免疫球蛋白超家族成员和归巢受体。浸润类风湿滑膜的T淋巴细胞表现出活化表型，其黏附受体的亲和力增加，导致这些细胞与细胞外基质蛋白（ECM）和细胞配体（VCAM-1、ICAMs）之间的相互作用增强。T细胞整合素与其配体的相互作用，除了额外的抗原刺激外，还可触发这些细胞的促有丝分裂反应，这一现象可能导致类风湿滑膜中观察到的细胞增多。此外，细胞通过整合素与ECM的附着会诱导几种蛋白酶的分泌，这些蛋白酶可能导致RA中观察到的组织损伤。对黏附受体在RA和其他炎症性疾病发病机制中作用的认识不断增加，将通过以下方式引入一种新的治疗方法：使用旨在干扰黏附分子功能的特异性阻断试剂。
