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(Circulation Research. 2000;86:281.)
© 2000 American Heart Association, Inc.

Integrative Physiology

Immunoglobulin Isotype Determines Pathogenicity in Antibody-Mediated Myocarditis in Naïve Mice

Anita P. Kuan, Lionel Zuckier, Li Liao, Stephen M. Factor, Betty Diamond

From the Departments of Microbiology and Immunology (A.P.K., L.L., B.D.), Nuclear Medicine (L.Z.), and Pathology (S.M.F.) of the Albert Einstein College of Medicine, Bronx, NY.

Correspondence to Betty Diamond, MD, Department of Microbiology and Immunology, 1300 Morris Park Ave, Bronx, NY 10461. E-mail diamond{at}aecom.yu.edu

Abstract—Antimyosin reactivity is associated with cardiac damage in autoimmune myocarditis, an inflammatory heart disease characterized by a cellular infiltrate in the myocardium and myocyte necrosis. We are interested in the pathogenicity of antimyosin antibodies and their ability to cause autoimmune myocarditis. We have shown that antimyosin antibodies of the IgG isotype will induce disease in the DBA/2 mouse. In the present study, we show that IgM antimyosin antibodies do not induce myocarditis; however, these same antibodies become pathogenic when converted to the IgG isotype. Although IgM antibodies can penetrate the myocardium during cardiac inflammation, they are usually less able to leave the vascular compartment and penetrate cardiac tissue, thus accounting for their lack of pathogenicity. Thus, antimyosin B cells may be potentially pathogenic only after antigen activation and heavy chain class switching or under conditions that alter vascular permeability in the heart.

Key Words: immunoglobulin isotype • myocarditis • pathogenicity

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