T cells in cardiac myosin-induced myocarditis.
Autoimmune myocarditis induced by immunization with cardiac myosin can be seen as a virus-free system to analyze the immunopathological mechanisms of certain forms of postinfectious heart disease. Immunodepletion studies have shown that in A.SW mice myosin-induced myocarditis is mediated by both CD4+ and CD8+ cells. The CD4+ subset is at least required for the induction of the autoimmune response, whereas the CD8+ subset seems to play a key role in mediating the myocardial injury. In addition, we found a bias concerning the TCR repertoire, because T cells within the inflammatory heart infiltrate almost exclusively use V beta 8 elements. Furthermore, recent serologic and immunohistologic studies indirectly suggest that the cardiac myocyte is not the target for the anti-myosin response. Rather, the primary target might consist in dendritic cells presenting myosin epitopes even under normal conditions.
Neu
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Department of Pediatrics, Medical School, University of Innsbruck, Austria.
Pummerer
C
C
Rieker
T
T
Berger
P
P
D000818:Animals; D001323:Autoantibodies / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology; D015329:Gene Rearrangement, T-Lymphocyte; D051379:Mice; D008815:Mice, Inbred Strains; D009205:Myocarditis / Q000276:immunology* / Q000473:pathology; D009206:Myocardium / Q000166:cytology / Q000276:immunology; D009218:Myosins / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics; D016176:T-Lymphocyte Subsets / Q000276:immunology*
D001323:Autoantibodies; D001324:Autoantigens; D016693:Receptors, Antigen, T-Cell, alpha-beta; D009218:Myosins