Abstract
It is known that several factors such as virus infection and autoimmune cause myocarditis. Therefore, mechanisms of its onset and recovery are predicted to greatly differ with the causes of myocarditis. However, the vast majority of myocarditis display severe pathological changes with inflammatory cells and the crosstalk of component cells with cytokines/chemokines is thought to be a common mechanism in any kind of myocarditis. In rat experimental autoimmune myocarditis (EAM), there are dendritic cells, macrophages, granulocytes, T cells, cardiomyocytes and non-cardiomyocytic non-inflammatory (NCNI) cells such as fibroblasts, smooth muscle cells and endothelial cells at sites of myocarditis lesions.
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