Azathioprine was shown to be effective in suppressing the onset of experimental autoimmune myasthenia gravis (EAMG) in rabbits injected with acetylcholine receptor (AChR) from Torpedo californica. The correlation between clinical effects and several immunologic parameters resulting from the immunosuppressive treatment was studied.

Administration of azathioprine for 5 months prevented the appearance of EAMG for at least 12 months, even after discontinuation of the treatment, in rabbits injected once with AChR. The suppressive effect of azathioprine was followed by a decreased cellular reactivity such as lymphocyte transformation and binding of AChR to macrophages, as well as a decreased humoral reactivity such as levels of total circulating antibodies and of cytophilic antibodies. Whereas the cellular and humoral sensitivities toward the immunizing Torpedo receptor were decreased, the reactivity against self AChR was essentially abolished. The strong effect on the autoimmune reactivity may assign some specificity to the treatment with azathioprine in affecting selectively certain cell populations. It is possible that immune responses directed against certain antigenic determinants that may be actively involved in the pathogenesis of EAMG are selectively more affected by azathioprine. The immunologic findings should prove useful in assessing and evaluating azathioprine treatment of the human disease.


This work was supported by the Los Angeles Chapter of the Myasthenia Gravis Foundation.

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