Myocarditis, or inflammation of the heart muscle, is a principle cause of heart disease in young adults, who are thus prone to heart failure. Frequently, myocarditis is accompanied by the presence of autoantibodies specific for heart muscle. But the presence of these antibodies alone is not sufficient to cause disease; other serum proteins are also involved in the pathogenic disease process. In the August issue of Nature Immunology (Vol. 2, No. 8, pp. 739-745), researchers at Johns Hopkins in Baltimore report on the role played by a serum protein, complement component C3, in causing myocarditis.
Complement proteins are among those serum proteins that protect against bloodstream invaders, such as bacteria or parasites, and act in concert with circulating antibodies. Multiple complement proteins exist and bind to foreign surfaces in a precise order, where they can either lyse the offending pathogen directly or recruit phagocytic cells, by releasing bits of their proteins, such as C3a, to clear the microbes. The latter process is critical for the development of myocarditis. Rose and colleagues found depletion of C3 early in the course of disease development prevented onset and severity of the resulting disease. Moreover, blocking the receptors on leukocytes for the C3 cleavage products also resulted in diminished disease severity. Thus, therapies aimed at the complement system may prove beneficial in treating autoimmune myocarditis as well as other autoimmune diseases.
Noel R. Rose
Johns Hopkins University
School of Medicine
Department of Pathology
720 Rutland Avenue
Baltimore, MD 21205
Tel: (+1) 410-955-0330
Fax: (+1) 410-955-0105
(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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