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Contributions made by B cell subsets to myasthenia gravis immune dysregulation
Authors: Panos A. Stathopoulos, Aditya Kumar, Steven Pan, Richard J. Nowak and Kevin C. O’Connor
Department of Neurology, Yale School of Medicine, New Haven, CT
Abstract
INTRODUCTION: Myasthenia gravis (MG) pathology is mediated by autoantibodies against acetylcholine receptors (AChR) or muscle-specific kinase (MuSK). The mechanisms underlying autoantibody production are not well understood.
OBJECTIVE: Identify the B cell subset(s) contributing to autoantibody production.
METHODS: Flow cytometry-based B cell immunophenotyping, B cell repertoire sequencing, in-vitro antibody expression and recombinant antibody construction were employed. Antibody specificity was tested with cell based and radioimmunoassays.
RESULTS: Circulating plasmablasts were elevated in a subset of patients with active disease. Abnormal clonal expansions of both memory B cells and plasmablasts were observed. Autoantigen specific cells were identified in the memory B cell compartment.
CONCLUSION: The B cell compartment is distorted in MG. Antigen specific memory B cells may feed autoantibody-secreting plasmablasts; suggesting a mechanism for the efficacy of anti-CD20 therapy.
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