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.
Recommended CitationDalakas, Marinos C and Meisel, Andreas, "Immunomodulatory effects and clinical benefits of intravenous immunoglobulin in myasthenia gravis." (2022). Department of Neurology Faculty Papers. Paper 288.
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