Huber S A
Department of Pathology, University of Vermont College of Medicine, Burlington 05405, USA.
Clin Immunol Immunopathol. 1997 May;83(2):93-102. doi: 10.1006/clin.1997.4342.
Infections (viruses, bacteria, protozoa, fungi) are major etiological factors causing clinical myocarditis and dilated cardiomyopathy. In many patients and symptom-free relatives antibodies and T cells reactive to heart antigens are detected, which implies that autoimmunity is probably a major pathogenic mechanism of cardiac injury. Animal models have been established to elucidate how infections initiate autoimmunity and how autoimmune mediators cause death or transient dysfunction of myocytes. Two major types of experimental models are discussed: adjuvant-induced myocarditis, in which animals are given multiple immunizations of heart proteins (myosin, adenine nucleotide translocator); and virus-induced myocarditis, in which animals are infected with the viruses predominantly associated with the human disease.