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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