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The Journal of Immunology, 2002, 169: 1077-1083.
Copyright © 2002 by The American Association of Immunologists

Resistance to Experimental Autoimmune Myasthenia Gravis in IL-6-Deficient Mice Is Associated with Reduced Germinal Center Formation and C3 Production1

Caishu Deng2, Elzbieta Goluszko, Erdem Tüzün, Huan Yang and Premkumar Christadoss3

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555

To provide direct genetic evidence for a role of IL-6 in experimental autoimmune myasthenia gravis (EAMG), IL-6 gene KO (IL-6-/-) mice in the C57BL/6 background were immunized with Torpedo californica acetylcholine receptor (AChR) and evaluated for EAMG. Only 25% of AChR-immunized IL-6-/- mice developed clinical EAMG compared to 83% of C57BL/6 (wild-type) mice. A significant reduction in the secondary anti-AChR Ab of IgG, IgG2b, and IgG2c, but not the primary or secondary IgM response was observed in AChR-immunized IL-6-/- mice, suggesting a possible defect in T cell help and class switching to anti-AChR IgG2 isotype. The AChR-specific lymphocyte proliferative response, IFN-{gamma}, and IL-10 production were suppressed in AChR-immunized IL-6-/- mice. EAMG resistance in IL-6-/- mice was associated with a significant reduction in germinal center formation and decreased serum complement C3 levels. The data provide the first direct genetic evidence for a key role of IL-6 in the autoimmune response to AChR and in EAMG pathogenesis.




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