Immunity in dilated cardiomyopathy.
Although several immunologic parameters have been found to be abnormal, their precise relationship to the cause of the disease remains unclear. It is believed that a virus initiating a bout of myocarditis may play a role in the perpetuation of the chronic phase, probably via immunologic mediation. A selection acquired defect or damage to a subpopulation of suppressor T lymphocytes is possible, providing the basis for the development of an autoimmune disorder. Studies in mice have shown a clear link between active viral myocarditis and the subsequent development of cardiomyopathy. However, the trigger mechanism that initiates the cardiomyopathy is still elusive. Specific antigens, possibly altered virus or damaged cardiac tissue, may be playing the role of the "hidden or cloistered" antigen in eliciting the immunologic reactions through a cytotoxic T-cell mechanism. Identification and isolation of the specific "antigen" in question could resolve the dilemmas about the immunopathogenesis of cardiomyopathy in humans.
D000818:Animals; D001323:Autoantibodies / Q000032:analysis; D002311:Cardiomyopathy, Dilated / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D002908:Chronic Disease; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D009205:Myocarditis / Q000276:immunology / Q000382:microbiology; D009206:Myocardium / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D014777:Virus Diseases / Q000150:complications
D001323:Autoantibodies