The Enemy Within: Immunologic Responses to Cardiac Tissue

Abstract

T cell-mediated and humoral immune responses to cardiac tissue can arise in the course of viral, bacterial and protozoan infections as a result of collagen vascular diseases and other types of cardiac injury. Specialized antigenpresenting cells in the heart can effectively stimulate T lymphocytes to react against antigens released by damaged myocytes. The threshold for activation of immune responses against cardiac tissue antigens seems to be high, reflecting the likelihood that induction of these responses requires persistent stimulation both with the inciting antigens and with agents, including cytokines, that evoke antigen nonspecific inflammation. The mechanisms by which immune responses to cardiac tissue are likely to develop in the course of certain infectious diseases are presented. Once established, immunologic responses to cardiac tissue antigens are notably difficult to control. Indeed, corticosteroids and nonsteroidal anti-inflammatory agents, under certain circumstances, can impair healing of inflammatory lesions in myocardium. Currently available methods for monitoring the progress of immune-mediated cardiac diseases and the shortcomings of available treatments for altering the natural history of these conditions are presented and discussed. Information is provided about new immunomodulatory agents, presently undergoing clinical trials, that are likely to be useful in treating immune-mediated cardiac diseases. Vaccination against some of the agents known to stimulate immune-mediated injury to cardiac tissue, including the M proteins of group A streptococci and certain strains of Coxsackie B virus, has been shown to be feasible in experimental animals. Further research is warranted to identify antigens that elicit autoreactive immune responses injuring heart tissue and discriminate these from antigens that will induce protective immunity against infectious agents provoking immune-mediated cardiac diseases.