HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dalakas, M. C. Search for Related Content PubMed PubMed Citation Articles by Dalakas, M. C.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

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.

This article has been cited by other articles:

				B. Tackenberg, I. Jelcic, A. Baerenwaldt, W. H. Oertel, N. Sommer, F. Nimmerjahn, and J. D. Lunemann Impaired inhibitory Fc{gamma} receptor IIB expression on B cells in chronic inflammatory demyelinating polyneuropathy PNAS, March 24, 2009; 106(12): 4788 - 4792. [Abstract] [Full Text] [PDF]

				S. von Gunten, A. Schaub, M. Vogel, B. M. Stadler, S. Miescher, and H.-U. Simon Immunologic and functional evidence for anti-Siglec-9 autoantibodies in intravenous immunoglobulin preparations Blood, December 15, 2006; 108(13): 4255 - 4259. [Abstract] [Full Text] [PDF]

				J. T. H. Van Asseldonk, L. H. Van den Berg, G. H. Wieneke, J. H. J. Wokke, and H. Franssen Criteria for conduction block based on computer simulation studies of nerve conduction with human data obtained in the forearm segment of the median nerve. Brain, September 1, 2006; 129(Pt 9): 2447 - 2460. [Abstract] [Full Text] [PDF]

				H. Koller, B. C. Kieseier, S. Jander, and H.-P. Hartung Chronic Inflammatory Demyelinating Polyneuropathy N. Engl. J. Med., March 31, 2005; 352(13): 1343 - 1356. [Full Text] [PDF]

				Y. Nishimoto, M. Koga, M. Kamijo, K. Hirata, and N. Yuki Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration Neurology, June 8, 2004; 62(11): 1939 - 1944. [Abstract] [Full Text] [PDF]

				M. C. Dalakas Intravenous Immunoglobulin in Autoimmune Neuromuscular Diseases JAMA, May 19, 2004; 291(19): 2367 - 2375. [Abstract] [Full Text] [PDF]

				D. Walk, L. Y.J. Li, G. J. Parry, and J. W. Day Rapid resolution of quadriplegic CIDP by combined plasmapheresis and IVIg Neurology, January 13, 2004; 62(1): 155 - 156. [Full Text] [PDF]