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Immune mediators in inflammatory heart disease: insights from a mouse model

M. Afanasyeva and N.R. Rose1

W. Harry Feinstone Department of Molecular Microbiology and Immunology and Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A.

1 Correspondence: Noel R. Rose, The Johns Hopkins University, Department of Pathology, Rutland Avenue, Ross Building, Room 659, Baltimore, MD 21205, U.S.A.

Abstract

Cardiac myosin-induced murine myocarditis provides a useful model for assessing the role of immune mediators in the development of inflammatory heart disease. Myocarditis is characterized by leucocyte infiltration, fibrosis, and cardiomyocyte death, which collectively lead to deterioration of both systolic and diastolic function as assessed by pressure-volume relations. In severe cases, disease progresses to dilated cardiomyopathy and heart failure. Key factors that promote disease include complement, tumour necrosis factor-alpha, interleukin-4, and interleukin-12. Factors found to supress myocarditis include interferon-gamma, interleukin-10, and cyotoxic T lymphocyte antigen-4. Final disease outcome is determined by the interplay of these immune mediators.

Key Words: Autoimmunity • cardiomyopathy • cytokines • knockout mice • myocarditis • pressure-volume relations


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 Am. J. Pathol.Home page
M. Afanasyeva, D. Georgakopoulos, D. F. Belardi, A. C. Ramsundar, J. G. Barin, D. A. Kass, and N. R. Rose
Quantitative Analysis of Myocardial Inflammation by Flow Cytometry in Murine Autoimmune Myocarditis: Correlation with Cardiac Function
Am. J. Pathol., March 1, 2004; 164(3): 807 - 815.
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