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 language | English (US) |
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Pages (from-to) | 739-745 |
Number of pages | 7 |
Journal | Nature immunology |
Volume | 2 |
Issue number | 8 |
DOIs | |
State | Published - 2001 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology