Genetic control of experimental autoimmune myasthenia gravis in mice. II. Lymphocyte proliferative response to acetylcholine receptor is dependent on Lyt-1⁺ 23^- cells

Autoantibodies to acetylcholine receptors (AChR) are demonstrable in approximately 90% of patients with acquired myasthenia gravis (MG) and are the major pathogenic cause of the defect in neuromuscular transmission that is characteristic of MG. Experimental autoimmune myasthenia gravis (EAMG) can be induced in animals by immunization with AChR and adjuvants. Induction of EAMG and of autoantibodies to AChR is T cell dependent. Studies in congenic mice revealed that susceptibility to EAMG is linked to the major histocompatibility complex. The lymphocyte proliferative response to AChR is controlled in congenic mice by gene(s) within the 1-A subregion. In this communication we present evidence that proliferation of lymphocytes from high responder B6 (H-2(b)) mice in response to AChR is dependent on T lymphocytes expressing Lyt-1 ⁺23^- phenotype.