The aim of this research is the elucidation of immunological mechanisms responsible for neurological dysfunction in organ-specific autoimmunity of the neuromuscular system. Two rat models will be employed in this analysis - experimental autoimmune myasthenia gravis (EAMG), in which humoral immune mechanisms are primarily implicated, and experimental autoimmune encephalomyelitis (EAE), in which cell-mediated immunity is primarily implicated. The effector roles of antibodies and cellular immune responses in the pathogenesis of those diseases will be examined by adoptive transfer studies in vivo and, using muscle cell targets, in vitro (for EAMG). Subpopulations of T-lymphocytes will be separated by physical criteria and their roles in inducing and regulating antibody and cellular immune responses to both AChR and myelin basic protein will e investigated by adoptive transfers in vivo. Immunologic mechanisms mediating genetically determined susceptibility to organ-specific autoimmunity will be analyzed. New information and investigative techniques will be applied to studying serum and lymphocytes from patients with myasthenia gravis. Analysis and comparison of autoimmune mechanisms in these two different model diseases should provide a rational basis for designing specific immunotherapy for patients with organ-specific autoimmunity.