Dai Sheng-Ming, Shan Zheng-Zheng, Xu Huji, Nishioka Kusuki
Department of Rheumatology and Immunology, Changhai Hospital, Second Military Medical University, 174 Changhai Road, Shanghai 200433, P R China.
Ann Rheum Dis. 2007 Nov;66(11):1411-8. doi: 10.1136/ard.2006.067793. Epub 2007 May 14.
Recent data are presented which indicate a critical role for interleukin (IL)-18 in rheumatoid arthritis (RA). The T cells and macrophages invading the synovium or in the synovial fluid are the chief cellular targets of IL-18 in RA. Neutrophils, dendritic cells and endothelial cells may also be cellular mediators of IL-18. The direct effect of IL-18 on fibroblast-like synoviocytes or chondrocytes may not be essential or important. In RA, IL-18, which is mainly produced by macrophages, activates T cells and macrophages to produce proinflammatory cytokines, chemokines, adhesion molecules and RANKL which, in turn, perpetuate chronic inflammation and induce bone and cartilage destruction.
近期数据表明白细胞介素(IL)-18在类风湿关节炎(RA)中起关键作用。侵入滑膜或滑膜液中的T细胞和巨噬细胞是RA中IL-18的主要细胞靶点。中性粒细胞、树突状细胞和内皮细胞也可能是IL-18的细胞介质。IL-18对成纤维细胞样滑膜细胞或软骨细胞的直接作用可能并非必不可少或重要。在RA中,主要由巨噬细胞产生的IL-18激活T细胞和巨噬细胞,使其产生促炎细胞因子、趋化因子、黏附分子和核因子κB受体活化因子配体(RANKL),进而使慢性炎症持续存在并导致骨和软骨破坏。