Cope Andrew P
The Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College London, Aspenlea Road, Hammersmith, London, W6 8LH, UK.
Arthritis Res Ther. 2008;10 Suppl 1(Suppl 1):S1. doi: 10.1186/ar2412. Epub 2008 Oct 15.
Over the past decade and a half, advances in our understanding of the pathogenesis of immune-mediated diseases such as rheumatoid arthritis (RA) have translated directly into benefit for patients. Much of this benefit has arisen through the introduction of targeted biological therapies. At the same time, technological advances have made it possible to define, at the cellular and molecular levels, the key pathways that influence the initiation and persistence of chronic inflammatory autoimmune reactions. As our understanding grows, it is likely that this knowledge will be translated into a second generation of biological therapies that are tailor-made for the patient. This review summarizes current perspectives on RA disease pathogenesis, with particular emphasis on what RA T cells look like, what they are likely to see, and how they contribute to persistence of the chronic inflammatory response.
在过去十五年中,我们对类风湿关节炎(RA)等免疫介导疾病发病机制的理解取得的进展已直接惠及患者。这种益处很大程度上源于靶向生物疗法的引入。与此同时,技术进步使我们能够在细胞和分子水平上确定影响慢性炎症性自身免疫反应起始和持续的关键途径。随着我们的理解不断深入,这些知识很可能会转化为为患者量身定制的第二代生物疗法。本综述总结了目前对RA疾病发病机制的观点,特别强调RA T细胞的样子、它们可能识别的物质,以及它们如何导致慢性炎症反应的持续。