CD20-mediated B cell depletion in acetylcholine receptor autoantibody-positive myasthenia gravis

P. Kanatas, Kevin C. O’Connor, P. Stathopoulos
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Abstract

Myasthenia gravis (MG) is an autoimmune disorder characterized by muscle weakness and fatigue, mediated in the majority of cases by IgG1 autoantibodies targeting the acetylcholine receptor (AChR). As AChR autoantibodies have been shown to be pathogenic, therapies targeting B cells have been applied in patients with AChR MG for more than a decade. Recently, a phase 2 trial of the CD20-targeting agent, rituximab, in AChR MG unfortunately failed to meet its primary endpoint. Converging data however from non-randomized clinical series, some of which with more participants than the phase 2 trial, support efficacy of rituximab in AChR MG, especially early onset disease. In this opinion article, we summarize both clinical data and mechanistic principles on the use of CD20 depletion therapy in AChR MG, which we believe lend support to the argument that CD20 depletion can still be a useful therapeutic strategy for patients with AChR MG.
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cd20介导的B细胞耗竭在乙酰胆碱受体自身抗体阳性的重症肌无力中
重症肌无力(MG)是一种以肌肉无力和疲劳为特征的自身免疫性疾病,在大多数情况下由靶向乙酰胆碱受体(AChR)的IgG1自身抗体介导。由于AChR自身抗体已被证明具有致病性,针对B细胞的治疗已经在AChR MG患者中应用了十多年。最近,一项针对cd20靶向药物利妥昔单抗(rituximab)治疗AChR MG的2期试验不幸未能达到其主要终点。然而,来自非随机临床系列的聚合数据,其中一些比2期试验的参与者更多,支持利妥昔单抗治疗AChR MG的疗效,特别是早发性疾病。在这篇观点文章中,我们总结了在AChR MG中使用CD20清除疗法的临床数据和机制原理,我们认为这支持了CD20清除对于AChR MG患者仍然是一种有用的治疗策略的观点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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