Autoimmunity in heart disease: mechanisms and genetic susceptibility.
Recent studies of heart disease suggest that immunologically mediated processes often accompany cardiac injury and can contribute to pathogenesis. Murine models of myocarditis have provided insight into the mechanisms by which autoimmune responses to cardiac antigens arise and cause tissue pathology. It is now evident that T cells, cytokines and antibodies can all contribute to cardiac injury. Furthermore, murine models have demonstrated that both the propensity to develop autoreactivity following cardiac injury and the vulnerability of the heart to these responses are under genetic control. Continued studies will help to identify susceptibility genes and might aid in the development of strategies to protect individuals at risk from immunologically mediated damage following cardiac injury.
Malkiel
S
S
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Kuan
A P
AP
Diamond
B
B
D000818:Animals; D001323:Autoantibodies / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D007150:Immunohistochemistry; D008285:Major Histocompatibility Complex; D051379:Mice; D009205:Myocarditis / Q000235:genetics / Q000276:immunology*; D009218:Myosins / Q000737:chemistry / Q000235:genetics / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies; D001324:Autoantigens; D016207:Cytokines; D009218:Myosins