Cardiac myosin induces myocarditis in genetically predisposed mice.

摘要: After infection with coxsackie virus B3 (CB3), H-2 congenic mice on an A- background develop immunologically mediated myocarditis associated increased titer of myosin autoantibody, part which is specific for the cardiac isoform. The present study demonstrates that itself induces severe and high titers autoantibodies in A/J, A.SW/SnJ, A.CA/SnJ mice. As CB3-induced myocarditis, one population these was myosin. A.BY/SnJ B10.A/SgSnJ also developed disease after immunization, but prevalence autoantibody were lower. In contrast, C57BL/6J C57BL/10J resistant to induced by did not or myosin-specific autoantibodies. Immunization skeletal muscle had no effect compared controls injected complete Freund's adjuvant, thereby suggesting immunogenic epitopes are unique Furthermore, we found susceptibility influenced major histocompatibility complex genes closely linked complex. Because there parallels between CB3, this new animal model can be used analyze pathologic mechanisms autoimmune heart disease.