Lundy Steven K, Sarkar Sujata, Tesmer Laura A, Fox David A
Department of Internal Medicine, Division of Rheumatology and Rheumatic Diseases Core Center, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.
Arthritis Res Ther. 2007;9(1):202. doi: 10.1186/ar2107.
Recent findings have substantiated the importance of T lymphocytes to the pathogenesis of rheumatoid arthritis (RA). Here, we review emerging data regarding genetic predisposition, spontaneous animal models of arthritis, and cell-cell interactions that implicate T cells as driving synovial inflammation and joint destruction. Information regarding the proinflammatory role of interleukin-17-producing T cells and the functional state of regulatory T cells both in animal models and in patients with RA is also discussed. In light of the overwhelming evidence that disrupted T-cell homeostasis greatly contributes to joint pathology in RA, the therapeutic potential of targeting activators of pro-inflammatory T cells or their products is compelling.
最近的研究结果证实了T淋巴细胞在类风湿关节炎（RA）发病机制中的重要性。在此，我们综述了有关遗传易感性、关节炎自发动物模型以及涉及T细胞驱动滑膜炎症和关节破坏的细胞间相互作用的新数据。还讨论了在动物模型和RA患者中，产生白细胞介素-17的T细胞的促炎作用以及调节性T细胞的功能状态的相关信息。鉴于大量证据表明T细胞内环境稳态的破坏极大地促成了RA的关节病变，靶向促炎T细胞激活剂或其产物的治疗潜力令人瞩目。
