摘要
TNF伪 is a cytokine that is central to the pathogenesis of several autoimmune diseases. More specifically, the deleterious effects of TNF伪 in rheumatoid arthritis (RA) are well established. The proinflammatory influence of TNF伪 in RA is related both to direct effects mediated by the induction of other proinflammatory cytokines, metalloproteinases, and free radicals; and to modulation of the regulatory T cells (Tregs). Furthermore, the TNF伪 antagonists used to treat RA can induce the emergence of a distinctive Treg subpopulation. Nevertheless, a recent body of data suggests that TNF伪 may also exert anti-inflammatory effects, which may be mediated in part via Tregs. TNF伪 binds to the TNF receptor 2 expressed preferentially at the Treg surface, thereby activating and promoting the development of Tregs. Data from patients with RA and more recent evidence obtained in the absence of disease are consistent with a paradoxical effect of TNF伪 on Tregs. TNF伪 may have different effects on naturally occurring Tregs and induced Tregs.