肿瘤坏死因子α（tumor necrosis factor alpha，TNFα）是一种具有多效生物活性的细胞因子，能够引起细胞凋亡、细胞增殖、分化、促炎症反应和免疫调节等作用。TNFα在类风湿关节炎（rheumatoid arthritis，RA）的致病机制中起关键作用。TNFα与TNF受体结合，能够引起细胞内的信号传导，通过复杂的级联反应和信号网络，激活转录因子核因子-κB（nuclear factor-kappa B，NF-κB）和活化蛋白-1（activator protein-1，AP-1），调控目的基因的表达，造成炎症反应和骨关节损伤。而以TNFα为靶位的药物已经被开发并应用于RA的临床治疗，通过阻断TNFα引起的信号传导来降低炎症反应被证明是安全有效的。本文就TNFα在类风湿关节炎病理机制中的作用及抗TNFα药物的进展作一综述。

Tumor necrosis factor alpha (TNFα) is a pleiotropic cytokine that mediates diverse biological effects, including apoptosis, cell proliferation, differentiation, proinflammatory reaction and immunoregulation. TNFα is known to play a critical role in the pathogenic mechanism of rheumatoid arthritis (RA). Binding of TNFα to TNF receptor ( TNFR) results in transduction of cellular signal. Through complex signaling cascades and networks, transcription factors NF-κB and AP-1 are activated to regulate target gene expression, resulting in joint inflammation and damage. Drugs targeting TNFα have been developed to reduce the injurious effects of proinflammatory cytokine and have proved to be safe and effective in the treatment of patients with RA. This article reviews the roles of TNFα in pathogenic of RA and the recent progress of anti-TNFα agents.