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*Myasthenia Gravis
The Journal of Immunology, 1998, 161: 2856-2862.
Copyright © 1998 by The American Association of Immunologists

The Th2 Cytokine IL-4 Is Not Required for the Progression of Antibody-Dependent Autoimmune Myasthenia Gravis1

Balaji Balasa*, Caishu Deng{dagger}, Jae Lee*, Premkumar Christadoss{dagger} and Nora Sarvetnick2,*

* Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037; and {dagger} Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555

Experimental autoimmune myasthenia gravis (EAMG), a disorder of the neuromuscular junction, is mediated by autoantibodies against muscle nicotinic acetylcholine receptor (AChR). The roles of IFN-{gamma} (Th1) and IL-4 (Th2) cytokines in the initiation and progression of this disease are not fully understood. Recently, we have demonstrated that IFN-{gamma} is necessary for the initiation of tAChR-induced EAMG in mice. However, the role of IL-4 in the progression of clinical EAMG remained undetermined. In this study we have addressed the contribution of IL-4 in the disease progression in IL-4-/- C57BL/6j mice whose IL-4 gene has been disrupted. Following immunization with Torpedo (t) AChR, the IL-4-/- mice readily developed signs of muscle weakness and succumbed to clinical EAMG with kinetics similar to the susceptibility of IL-4+/+ mice. The tAChR-primed lymph node cells from IL-4-/- mice vigorously proliferated to tAChR and to its dominant {alpha}146–162 sequence associated with disease pathogenesis. However, these T cells secreted higher levels of IFN-{gamma} and IL-2, suggesting the development of a Th1 default pathway in these mice. Nevertheless, the IL-4 mutation had no effect on the recruitment of CD4+ Vß6+ T cells specific to the dominant tAChR {alpha}146–162 sequence in vivo. Immune sera from IL-4-/- mice showed a dramatic increase in mouse AChR-specific IgG2a levels followed by a concomitant decrease in IgG1 levels, but these mice did not exhibit an accelerated disease. In conclusion, we have demonstrated for the first time that IL-4 is not required either for the generation of a pathogenic anti-AChR humoral immune response or for progression of clinical EAMG in mice.




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