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Department of Neurology, Kanazawa University School of Medicine (Dr. Takamori), Kanazawa, and the First Department of Internal Medicine, Nagasaki University School of Medicine (Dr. Ide). Nagasaki, Japan.
The effects of prostaglandin E1 (PGE1), a potent inhibitor of lymphocyte functions, were studied in rats immunized with acetylcholine receptor (AChR) to induce experimental autoimmune myasthenia gravis (EAMG). Daily injections of PGE1, 400 µg per day, prevented the development of acute EAMG, which is attributed to antibody-dependent, complement-mediated cytolysis. This was associated with suppression of delayed-type cutaneous hypersensitivity response to AChR. PGE, did not prevent the subsequent onset of chronic EAMG, which reflects accelerated degradation of AChR by antibody and complement-mediated cell lysis in the postsynaptic membrane.
Address correspondence and reprint requests to Dr. Takamori, Department of Neurology, Kanazawa University School of Medicine, 13-1, Takara-machi, Kanazawa, Japan 920.
This investigation was supported in part by research grants funded by the Japanese Ministry of Education (56480173), and Neuroimmunological Disorders Research Committee, Japanese Ministry of Health and Welfare.
Accepted for publication September 21, 1981.
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