Immunologic aspects of heart disease.
All forms of heart disease, whether caused by streptococcus group A, aseptic heart injury, virus, hypersensitivity, autoimmune conditions, or graft-versus-host reactions, have in common allogenic transformation of the myocardial cell membrane and production of multifunctional autoantibodies, in addition to cause-specific antibodies, some of which cross-react with heart tissue. The outcome of this immunologic insult depends on the ability of the host's immunoregulatory mechanisms to dispose swiftly of the offending antigen and antibody or their complexes. Heart disease often results when these mechanisms, exemplified here, are not intact or when they function inappropriately in genetic or acquired settings and in varying haplotype frames.
D001161:Arteriosclerosis / Q000276:immunology; D009202:Cardiomyopathies / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D004697:Endocarditis, Bacterial / Q000276:immunology; D006331:Heart Diseases / Q000276:immunology*; D006335:Heart Injuries / Q000276:immunology; D006801:Humans; D006942:Hypergammaglobulinemia / Q000276:immunology; D006968:Hypersensitivity, Delayed; D006969:Hypersensitivity, Immediate; D012214:Rheumatic Heart Disease / Q000276:immunology; D013290:Streptococcal Infections / Q000276:immunology; D013297:Streptococcus pyogenes / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology