Nature Immunology
2, 739 - 745 (2001)
doi:10.1038/90686
Contribution of the innate immune system to autoimmune myocarditis: a role for complementZiya Kaya1, Marina Afanasyeva1, 2, Yan Wang1, K. Malte Dohmen1, Jens Schlichting1, Theresa Tretter3, DeLisa Fairweather1, 2, V. Michael Holers4
& Noel R. Rose1, 21
Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. 2
The W. Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. 3
Department of Molecular Biology and Genetics, The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. 4
Departments of Medicine and Immunology, University of Colorado Health Science Center, Denver, CO 80262, USA.
Correspondence should be addressed to Noel R. Rose nrrose@jhsph.eduMyocarditis is a principal cause of heart disease among young adults and is often a precursor of heart failure due to dilated cardiomyopathy. We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type 1 (CR1) and type 2 (CR2). We also found a subset of CD44hiCD62Llo T cells that expresses CR1 and CR2 and propose that both receptors are involved in the expression of B and T cell activation markers, T cell proliferation and cytokine production. These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction of an autoimmune disease.
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