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Issue 1110 coverAutoimmunity, Part B Novel Applications of Basic Research Volume 1110 published September 2007
Ann. N.Y. Acad. Sci. 1110: 550–558 (2007). doi: 10.1196/annals.1423.059
Copyright © 2007 by the New York Academy of Sciences
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Part II. Treatment

Suppression of Experimental Autoimmune Myasthenia Gravis by Intravenous Immunoglobulin and Isolation of a Disease-Specific IgG Fraction

SARA FUCHSa, TALI FEFERMANa, KAI-YUN ZHUa, ROBERTO MEIDLERb, RAANAN MARGALITa, NINGSHAN WANGa, ORGAD LAUBb AND MIRIAM C. SOUROUJONa,c

a Department of Immunology, the Weizmann Institute of Science, Rehovot, Israel b Omrix Biopharmaceuticals, Nes-Ziona, Israel c Department of Natural Sciences, The Open University of Israel, Raanana, Israel

Key Words: myasthenia gravis • (MG) • experimental autoimmune myasthenia gravis (EAMG) • intravenous immunoglobulin • (IVIG) • immunotherapy

Address for correspondence: Sara Fuchs, Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. Voice: +972-8-9342618; fax: +972-8-9344141.  sara.fuchs{at}weizmann.ac.il

Intravenous immunoglobulin (IVIG) administration has been beneficially used for the treatment of a variety of autoimmune diseases including myasthenia gravis (MG). We have demonstrated that IVIG administration in experimental autoimmune MG (EAMG) results in suppression of disease that is accompanied by decreased Th1 cell and B cell proliferation. Chromatography of pooled human immunoglobulins (IVIGs) on immobilized IgG, isolated from rats with EAMG, results in a complete depletion of the suppressive activity of the IVIG. Moreover, the eluate from this EAMG-specific antibody column retains the immunosuppressive activity of IVIG. This study supports the notion that the therapeutic effect of IVIGs is mediated by an antigen-specific anti-immunoglobulin (anti-idiotypic) activity that is essential for its suppressive activity.




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S. FUCHS, T. FEFERMAN, R. MEIDLER, R. MARGALIT, C. SICSIC, T. BRENNER, O. LAUB, and M. C. SOUROUJON
Immunosuppression of EAMG by IVIG Is Mediated by a Disease-specific Anti-immunoglobulin Fraction
Ann. N.Y. Acad. Sci., June 1, 2008; 1132(1): 244 - 248.
[Abstract] [Full Text] [PDF]



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