The immune response following myocardial infarction: a role for T-cell-mediated myocyte damage.

Myocardial damage by inflammatory cells has been The myocyte injury could be prevented by CD8 antibodies, indicating that the myocytolysis reimplicated in a broad range of muscle diseases including cardiac transplant rejection, viral myquired CD8+ CTLs. In this experiment, the myocyte injury was directed against myocytes derived from ocarditis, and ischemic heart disease. In each of these diseases it has been demonstrated that inthe same strain as the donor heart, whereas there was not a significant myocytopathic effect when flammation is activated and that the immune cells can induce myocyte damage, but the potential the splenocytes were incubated with myocytes from the recipient. This is an important characteristic beneficial or detrimental effect of the immune response against the myocardium is only partially that is different in models that involve alloantigens as opposed to autoantigens as proposed in other understood. In this issue, Varda-Bloom et al. provide evidence for lymphocyte-mediated myocyte cell models of myocyte injury. Viral myocarditis is another disease that is chardamage following myocardial infarction in the rat. These findings, in the context of other studies reacterized by marked T-cell infiltration. Both direct viral injury and the immune response of the host garding the immune mechanisms of cardiac damage, form a framework for future studies on the play an important role in the pathogenesis of viral heart disease. Results from experiments in murine potential significance of lymphocyte-mediated myocardial injury following myocardial infarction. models of viral myocarditis indicate that although the immune response has an important protective Of the immune-related cardiac diseases, allograft cardiac transplantation is the best characterized. role, it may also have deleterious effects on the host. The balance between these protective and deleterious Allograft transplantation exposes the recipient to foreign antigens to which the immune cells respond effects may ultimately determine the course of disease after enteroviral infection. Evidence for a pathogenic appropriately. While the immune response to allograft transplantation is complex, there are conrole for the immune response has been reviewed elsewhere. This includes evidence that CTLs from siderable experimental data implicating a role for CD8+ cytotoxic T-lymphocyte (CTL)-mediated Coxsackievirus B3-infected mice can induce a cytopathic effect in uninfected, syngeneic-cultured myocyte injury in transplant rejection. This includes the fact that CD8+ CTLs comprise a sigmyocytes. Furthermore, adoptive T-cell transfer experiments have shown that lymphocytes from nificant fraction of the cellular infiltrate in allografts that are undergoing the rejection process. In adinfected mice are able to induce myocarditis in recipient uninfected mice. These findings suggest a dition, it has been shown that activated splenocytes from mice that had received a cardiac allograft can potentially detrimental role for the immune response in viral-mediated heart disease. injure cardiac myocytes in an allospecific manner.