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Brief description/objective

The exact pathological basis of human myocarditis has not yet been sufficiently clarified and therefore, the appropriate treatment has remained a major clinical problem. Assuming that immunopathological damage contributes to the inflammatory nature of this disease, it has been suggested that immunosuppressive treatment might be beneficial for the patients. Furthermore, a number of different approaches for antigen-specific downregulation of heart-reactive immune reactions have been evaluated, but have failed to achieve complete myosin-specific immune tolerance and to influence the course of infection-associated myocarditis. The genetic approach outlined in this proposal will not only provide a powerful tool to study the cellular basis on autoimmune myocarditis, but will also generate a better understanding of the molecular mechanisms involved in cardiac autoimmunity. We believe that this new mouse model will be useful to develop effective intervention strategies for autoimmune myocarditis.