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Journal of Experimental Medicine, Vol 181, 1123-1131, Copyright © 1995 by Rockefeller University Press
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L Liao, R Sindhwani, M Rojkind, S Factor, L Leinwand and B Diamond
Albert Einstein College of Medicine, Bronx, New York 10461.
Injury to cardiac myocytes often leads to the production of anti-myosin antibodies. While these antibodies are a marker of myocardial injury, their contribution to pathogenesis in diseases such as autoimmune myocarditis or rheumatic fever is much less clear. We demonstrate in this report that monoclonal anti-myosin antibodies can mediate myocarditis in a susceptible mouse strain. Additionally, we show disease susceptibility depends on the presence of myosin or a myosin- like molecule in cardiac extracellular matrix. This study demonstrates that susceptibility to autoimmune heart disease depends not only on the activation of self-reactive lymphocytes but also on genetically determined target organ sensitivity to autoantibodies.
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