类风湿关节炎B淋巴细胞耗竭:靶向CD20。

Jonathan C W Edwards, Maria J Leandro, Geraldine Cambridge
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引用次数: 52

摘要

背景:在20世纪90年代,有证据表明类风湿关节炎(RA)的B淋巴细胞减少可能是主要的益处。方法与结果:1997年,B淋巴溶解单克隆抗cd20抗体利妥昔单抗问世。最初是在伦敦大学学院的公开研究中,最近在一项多中心随机对照试验中,已经证明了显著的临床疗效。伦敦大学学院(University College London)的40名RA患者目前共接受了75个治疗周期的利妥昔单抗(最多4个单独)或皮质类固醇、环磷酰胺和/或甲氨蝶呤联合治疗。这些患者正在进行的免疫动力学研究揭示了一些关于B细胞靶向治疗潜力和RA发病机制的问题。结论:B淋巴细胞耗竭的影响越来越支持RA的炎症效应机制和潜在的免疫调节紊乱是由自身抗体而不是T细胞驱动的这一观点。
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B lymphocyte depletion in rheumatoid arthritis: targeting of CD20.

Background: During the 1990s evidence emerged to suggest that B lymphocyte depletion in rheumatoid arthritis (RA) might be of major benefit.

Methods and results: In 1997 the B lympholytic monoclonal anti-CD20 antibody rituximab became available. Significant clinical efficacy has been demonstrated in RA, initially in open studies at University College London and recently in a multicentre randomised controlled trial. Forty RA patients at University College London have now received in total 75 treatment cycles with rituximab (up to 4 individually) alone or in combination with corticosteroid, cyclophosphamide and/or methotrexate. Ongoing immunodynamic studies of these patients have shed light on a number of questions about both the therapeutic potential of B cell targeting, and the pathogenesis of RA.

Conclusions: The effects of B lymphocyte depletion lend increasing support to the idea that both the inflammatory effector mechanism and the underlying immunoregulatory disturbance in RA are driven by autoantibody rather than T cells.

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