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C5 complement inhibition contributes to increased proliferative activity and antigen specific recall response in experimentally acquired myasthenia gravis (EAMG)

Background: Myasthenia gravis (MG) is an autoimmune disorder caused by the production of autoantibodies against the acethylcholine receptor (AChR). Antibodies bind to the AChR and activate the complement system leading to the destruction of neuromuscular junction (NMJ). Experimentally acquired MG (EAMG) rats were used to investigate the therapeutic role of C5 complement inhibitor, rEV576.