Lennon_1976_Ann.N.Y.Acad.Sci_274_283

Rats inoculated intradermally with eel acetylcholine receptor protein(AChR) with adjuvants developed autoimmunity to skeletal muscle AChR. This is evidenced clinically as two episodes of experimental autoimmune myasthenia gravis (EAMG), an acute phase that occurs early (8 days) and is transient, and a chronic phase (30 days) that is usually progressive. Positive delayed cutaneous reactivity appeared at day 4 and serum antibody to eel AChR was detectable by day 7 postinoculation. After day 25 the titer of antibody to syngeneic muscle AChR rose abruptly. Antibody to muscle AChR sedimented as 7S. Lymph node cells from rats sensitized to AChR were capable of transferring EAMG to normal recipients. Thymectomy after the onset of EAMG had no effect. Early treatment in vivo with antithymocyte serum suppressed acute but not chronic phase EAMG. Experiments combining thymectomy, x-irradiation and reconstitution with distinct populations of lymphocytes indicated athat thymus-derived lymphocytes are required for induction of EAMG and antibody to AChR. These data suggest that both cellular and humoral responses to AChR, either sequentially or in combination, contribute to the pathogenesis of EAMG.