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TNF-related apoptosis-inducing ligand (TRAIL) in rheumatoid arthritis: what's new?

机译:类风湿关节炎中与TNF相关的凋亡诱导配体(TRAIL):有何新变化?

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TNF-related apoptosis-inducing ligand (TRAIL) is a type II transmembrane protein of the TNF superfamily that serves as an extracellular signal that triggers programmed cell death in tumor cells, without affecting normal cells. Recently, scientists have turned their attention to the emerging role of TRAIL in immune and autoimmune responses. TRAIL has been shown to down-regulate the self-antigens in autoimmune diseases, such as rheumatoid arthritis (RA) by exerting its apoptotic effect on activated T cells and synoviocytes and by its local anti-inflammatory effect. The impact of TRAIL molecular variants and agonistic monoclonal antibodies in the regulation of TRAIL activity in arthritis animal models strongly supports the idea of testing the role of TRAIL in humans, with the aim of developing new effective therapies that promote apoptosis of synoviocytes and/or infiltrating lymphocytes, by targeting TRAIL. The aim of this review is to summarize recent progress and current knowledge of TRAIL functions in RA.
机译:TNF相关凋亡诱导配体(TRAIL)是TNF超家族的II型跨膜蛋白,可作为细胞外信号,触发肿瘤细胞中程序性细胞死亡,而不会影响正常细胞。最近,科学家将注意力转向TRAIL在免疫和自身免疫反应中的新兴作用。 TRAIL已显示出通过自身对活化T细胞和滑膜细胞的凋亡作用以及其局部抗炎作用而下调自身免疫疾病(例如类风湿性关节炎(RA))中的自身抗原。 TRAIL分子变体和激动性单克隆抗体对关节炎动物模型中TRAIL活性调节的影响,强烈支持了测试TRAIL在人类中的作用的想法,目的是开发能够促进滑膜细胞凋亡和/或浸润的新有效疗法。通过靶向TRAIL获得淋巴细胞。这篇综述的目的是总结RA中TRAIL功能的最新进展和当前知识。

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