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Department of Neurology and Neuromuscular Research Laboratory, Mayo Clinic, Rochester, MN.
To clarify the role of cell-mediated versus humoral immune effector responses in myasthenia gravis (MG), we examined the occurrence of inflammatory cells in muscle from 30 patients with MG, determined the site of accumulation of the cells (at or remote from end-plates), enumerated and immunophenotyped those cells at the end-plate, and evaluated the frequency of deposition of the complement membrane attack complex (MAC) at the end-plate. Seven of 30 patients had well-defined collections of mononuclear cells in muscle (lymphorrhages), but these were not topographically related to the end-plates. Twenty of 30 patients had inflammatory cells (mostly macrophages and T cells) at or near end-plates, but these cells were present at less than 10% of the end-plates, and only seldom was there more than one cell at any end-plate. None of the inflammatory cells penetrated the muscle fiber near the end-plate. All end-plates of all patients immunostained for MAC. The findings reconfirm that the predominant immune effector response in MG is humorally mediated. The lymphorrhages in muscle and other tissues are probably a nonspecific indicator of disturbed immune regulation in MG.
Address correspondence and reprint requests to Dr. Andrew G. Engel, Department of Neurology, Mayo Clinic, Rochester, MN 55905.
Supported by NIH grant NS6277 and a grant from the Muscular Dystrophy Association.
Received August 21, 1992. Accepted for publication in final form October 16, 1992.
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