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Use of monoclonal antiacetylcholine receptor antibodies to investigate the macrophage inflammation of acute experimental myasthenia gravis

Refractoriness to a second episode of acute disease

From the West Virginia University Medical Center, Department of Neurology (Dr. Corey), Morgantown, WV; and the Department of Neurology and The Committee irn Immunolow (Drs. Richman, Shuman, Gomez, and Arnason), The Division of the Biological Sciences and The Pritzker School of Medicine. The University of Chicago, Chicago. IL.

The acute phase of experimental autoimmune myasthenia gravis (EAMG) is characterized by macrophage inflammation of muscle endplates and by muscle fiber necrosis. We induced acute EAMG by passive transfer of monoclonal antibodies (mAbs) directed against the acetylcholine receptor (AChR) to investigate this brief and self-limited disorder. After the initial acute phase, animals were refractory to induction of a second episode by subsequent injection of the same mAb, or another anti-AChR mAb of different idiotype and which binds to a separate epitope. Therefore, the refractory state was not caused by an anti-idiotypic response or elpitopic modulation. Adoptive transfer of spleen cells from refractory animals had no effect, excluding a role of suppressor lymphocytes, and there was no evidence from-experiments involving adoptive transfer of spleen cells from naive animals to refractory animals that refractory animals lacked effector cells.

Address correspondence and reprint requests to Dr. Corey, Department of Neurology, West Virginia University Medical Center, 103G Basic Sciences Building, Morgantown, WV 26506.

Supported in part by grants from the Muscular Dystrophy Association and National Institutes of Health (NS15462, NS07113. NS19779).

Accepted for publication January 28, 1985.