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

被引：138

作者：

Kaya, Z

Afanasyeva, M

Wang, Y

Dohmen, KM

Schlichting, J

Tretter, T

Fairweather, D

Holers, VM

Rose, NR ^{[1
]}

机构：

[1] Johns Hopkins Sch Med, Dept Pathol, Baltimore, MD 21205 USA

[2] Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA

[3] Johns Hopkins Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA

[4] Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA

[5] Univ Colorado, Hlth Sci Ctr, Dept Immunol, Denver, CO 80262 USA

来源：

NATURE IMMUNOLOGY | 2001年 / 2卷 / 08期

关键词：

D O I：

10.1038/90686

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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 (CRI) and type 2 (CR2). We also found a subset of CD44(hi)CD62L(lo)T cells that expresses CR 1 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.

引用

页码：739 / 745

页数：7

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[1] Experimental autoimmune myocarditis in A/J mice is an interleukin-4-dependent disease with a Th2 phenotype [J].