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Cellular immunity to acetylcholine receptor in myasthenia gravis

Relationship to histocompatibility type and antigenic site

Department of Neurology, Division of Biological Sciences, and Pritzker School of Medicine, The University of Chicago, Chicago, Illinois, and the Department of Neurobiology, Salk Institute, San Diego, California.

To debermine the nature of the cellular immune response directed against acetylcholine receptor in myasthenia gravis, we compared lymphocyte stimulation by eel receptor with clinical factors. The mean (k SEM) stimulation index wa.s 4.5 ± 0.9 for 39 myasthenic patients and 0.97 ± 0.18 for 48 controls (p < 0.001). Positive response in patients was associated with disease onset after 50 years (10 of 13 patients) and presence of thymoma (seven of eight patients), but not with HLA type. Stimulation index correlated with disease activity (rs = 0.6 3, < 0.01). Blocking the active portion of the receptor molecule with naja toxin resulted in 68 percent diminution of the response, suggesting that this site plays a significant role in the cellular immune response in myasthenia gravis.

Requests for reprints should be addressed to Dr. Richman, Department of Neurology, University of Chicago, 950 E. 59th Street, Chicago, IL 60637.

This work was supported in part by a Kermit E. Osserman Post-Doctoral Fellowship of the Myasthenia Gravis Foundation, Inc., and by grants from the Muscular Dystrophy Association of America, Inc., The National Institutes of Health (NS13426) and (NS11635), and the National Multiple Sclerosis Society (No. 1130).

Presented in part at the twenty-ninth annual meeting of the American Academy of Neurology, Atlanta, Georgia, April 1977.

Accepted for publication July 5, 1978.

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