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Mechanisms of action of IVIg and therapeutic considerations in the treatment of acute and chronic demyelinating neuropathies

From the National Institutes of Health, Bethesda, MD.

Address correspondence and reprint requests to Dr. Marinos C. Dalakas, National Institutes of Health, Building 10, Room 4N248, 10 Center Drive MSC 1382, Bethesda, MD 20892-1382.

Intravenous immunoglobulin (IVIg) is an immunomodulating agent that has multiple activities, including modulation of complement activation products, suppressing idiotypic antibody, saturating Fc receptors on macrophages, and suppressing various inflammatory mediators including cytokines, chemokines, and metalloproteinases. Because all these factors are implicated to various degrees in the pathogenesis of immune-mediated demyelination of the PNS, administration of IVIg could be beneficial in treating neuropathies by suppressing the immune-mediated processes that are directed against myelin or axonal antigenic targets. This article outlines the actions of IVIg in CIDP and other autoimmune neuropathies based on data derived from in vivo and in vitro studies. The predominant mechanisms by which IVIg exerts its action on these neuropathies appear to be a combined effect on complement inactivation, neutralization of idiotypic antibodies, cytokine inhibition, and saturation of Fc receptors on endoneurial macrophages.

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