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This article is the author's final published version in Expert Review in Neurotherapeutics, Volume 22, Issue 4, April 2022, Pages 313 - 318.

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Copyright © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (, which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.


Introduction Myasthenia gravis (MG) is an antibody-mediated disease that develops in the majority of patients mainly as a result of acetylcholine receptor (AChR) autoantibodies. This process is mediated by a series of immunoregulatory events. Therapeutic targets for MG include suppression of circulating antibodies or antibody production, suppression of complement activation, and immunomodulation of cytokines or T cells. Intravenous immunoglobulin (IVIg) has an effect on all of these mechanisms. Areas covered This narrative review explores the broad immunomodulatory effects of IVIg in MG and provides an update on IVIg treatment for MG. Expert opinion IVIg has a range of immunomodulatory effects on therapeutic targets relevant to the immunopathogenesis of MG. An emerging area of research is the pharmacogenomics of IVIg in MG related to FcRn and IgG catabolism. New data suggest that the FcRn VNTR3 genotype can affect the efficacy of IVIg in certain MG patients and may have an impact on IgG kinetics and selected dosing. Immune globulin 10% caprylate/chromatography purified (IVIg-C) has been shown to reverse the symptoms of severe acute exacerbation in patients with MG supporting its use for this severely ill subgroup of patients during a relapse.

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