Thalhamer T, McGrath M A, Harnett M M
Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, 120 University Place, Glasgow G12 8TA, UK.
Rheumatology (Oxford). 2008 Apr;47(4):409-14. doi: 10.1093/rheumatology/kem297. Epub 2008 Jan 10.
Rheumatoid arthritis (RA) is a chronic autoimmune disease in which imbalances in pro- and anti-inflammatory cytokines promote the induction of autoimmunity, inflammation and joint destruction. The importance of inflammatory cytokines in the pathogenesis of RA has been underscored by the success of biologics that act to block the effects of cytokines, such as tumour necrosis factor-alpha, interleukin (IL)-1 or IL-6, in treating disease. Mitogen-activated protein kinases (MAPKs) have been implicated as playing key regulatory roles in the production of these pro-inflammatory cytokines and downstream signalling events leading to joint inflammation and destruction. This article reviews the evidence that MAPKs play important roles in the pathogenesis of RA and discusses their therapeutic potential as drug targets.
类风湿关节炎（RA）是一种慢性自身免疫性疾病，其中促炎细胞因子和抗炎细胞因子的失衡会促进自身免疫、炎症和关节破坏的发生。作用于阻断细胞因子（如肿瘤坏死因子-α、白细胞介素（IL）-1或IL-6）作用的生物制剂在治疗疾病方面取得的成功，凸显了炎性细胞因子在RA发病机制中的重要性。丝裂原活化蛋白激酶（MAPK）被认为在这些促炎细胞因子的产生以及导致关节炎症和破坏的下游信号传导事件中发挥关键调节作用。本文综述了MAPK在RA发病机制中发挥重要作用的证据，并讨论了它们作为药物靶点的治疗潜力。
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