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Rituximab-induced B cell depletion in autoimmune diseases: potential effects on T cells.

机译:利妥昔单抗在自身免疫性疾病中诱导的B细胞耗竭:对T细胞的潜在影响。

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摘要

Peripheral B cell depletion strategies have been employed recently in the treatment of systemic autoimmune diseases and the initial clinical results have been encouraging. Although the major target of rituximab-based treatments was to reduce the levels of circulating autoantibodies, additional mechanisms of action may operate. Recent studies have addressed the question of potential effects of transient B cell depletion on other, non-B cell populations. The data, albeit uncontrolled, suggest that anti-CD20 monoclonal antibody treatment is associated with significant effects in the T cell pool, whereas individual clinical responses do not always correlate with changes in autoantibody titers. More specifically, it has been reported that rituximab administration may decrease the activated phenotype of peripheral and tissue-resident T cells by abolishing antigen presentation by B cells, and may enhance the numbers and function of regulatory T cells. In this review we analyze and discuss available data emerging from B cell depletion studies in patients with systemic lupus erythematosus, rheumatoid arthritis and other autoimmune conditions. Further controlled studies are needed to confirm the role of B cell depletion in modifying T cell function in vivo.
机译:外周血B细胞清除策略最近已用于全身性自身免疫性疾病的治疗,并且最初的临床结果令人鼓舞。尽管基于利妥昔单抗的治疗的主要目标是降低循环自身抗体的水平,但其他作用机制可能起作用。最近的研究已经解决了瞬时B细胞耗竭对其他非B细胞群体的潜在影响的问题。该数据尽管不受控制,但表明抗CD20单克隆抗体治疗与T细胞库中的显着作用有关,而个别临床反应并不总是与自身抗体滴度的变化相关。更具体地,已经报道了利妥昔单抗的施用可以通过消除B细胞的抗原呈递而降低外周和组织驻留T细胞的活化表型,并且可以增强调节性T细胞的数量和功能。在这篇综述中,我们分析和讨论了系统性红斑狼疮,类风湿性关节炎和其他自身免疫性疾病患者B细胞耗竭研究中出现的可用数据。需要进一步的对照研究来证实B细胞耗竭在体内修饰T细胞功能中的作用。

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