@article{oai:niigata-u.repo.nii.ac.jp:00006603, author = {Kodama, Makoto and Izumi, Tohru}, issue = {1}, journal = {Acta medica et biologica, Acta medica et biologica}, month = {Mar}, note = {Recently, we have established a novel experimental model for autoimmune myocarditis. Acute serious myocarditis can be induced in Lewis rats by immunization with cardiac myosin. This experimental\nmyocarditis is characterized by congestive heart failure. As is the case of acute myocarditis in humans, massive pericardial effusion, swelling and discoloration of the cardiac wall can be observed in this model. The lesions are composed of various inflammatory components, such as neutrophils, lymphocytes, macrophages, fragments of degenerated myofibers and interstitial edema. A considerable number of multinucleated giant cells are also observed in the lesions. This myocarditis is transferable in syngeneic naive rats by injection with concanavalin A-activated spleen cells obtained from previously immunized rats. On the other hand, the immunoglobulin fraction from rats with severe myocarditis is unable to transfer the myocarditis. Immunohistochemically, the cell infiltrates are mainly composed of macrophages and CD4+ T cells. Other populations of T cells are scarce and B cells are absent from this myocarditis. Microscopically, multinucleated giant cells were of two types, these being macrophage-like and myocyte-like in appearance. Immunohistochemically, both of them were stained with only OX42, a macrophage marker, and were not stained with an antidesmin antibody nor any lymphocyte markers. Consequently, we deduced that this experimental myocarditis is mediated by T cells. This model is expected to provide important information for the pathogenesis of human myocarditis.}, pages = {1--10}, title = {Experimental Autoimmune Myocarditis}, volume = {39}, year = {1991} }