Contribution of the innate immune system to autoimmune myocarditis: A role for complement

Ziya Kaya, Marina Afanasyeva, Yan Wang, K. Malte Dohmen, Jens Schlichting, Theresa Tretter, De Lisa Fairweather, V. Michael Holers, Noel R. Rose

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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 I (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.

Original languageEnglish (US)
Pages (from-to)739-745
Number of pages7
JournalNature immunology
Volume2
Issue number8
DOIs
StatePublished - Aug 25 2001

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Kaya, Z., Afanasyeva, M., Wang, Y., Dohmen, K. M., Schlichting, J., Tretter, T., Fairweather, D. L., Holers, V. M., & Rose, N. R. (2001). Contribution of the innate immune system to autoimmune myocarditis: A role for complement. Nature immunology, 2(8), 739-745. https://doi.org/10.1038/90686