Abstract
Myocarditis 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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Acknowledgements
We thank P. Caturegli, E. A. Stafford, M. V. Talor, W. M. Baldwin III, S. Mirshahidi and C. L. Burek for critically reading the manuscript and for technical advice. Supported by NIH grants ES07141, HL33878, HL65100 (to N. R. R.) and AI31105 (to V. M. H.). Z. K. was supported by the Deutsche Herzstiftung. T. T. was supported by the Deutsche Forschungsgemeinschaft.
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Kaya, Z., Afanasyeva, M., Wang, Y. et al. Contribution of the innate immune system to autoimmune myocarditis: a role for complement. Nat Immunol 2, 739–745 (2001). https://doi.org/10.1038/90686
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DOI: https://doi.org/10.1038/90686
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