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

doi:10.1038/90686

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

Cardiovascular Diseases

Research output: Contribution to journal › Article › peer-review

141 Scopus citations

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 CD44^hiCD62L^lo 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)
Pages (from-to)	739-745
Number of pages	7
Journal	Nature immunology
Volume	2
Issue number	8
DOIs	https://doi.org/10.1038/90686
State	Published - 2001

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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title = "Contribution of the innate immune system to autoimmune myocarditis: A role for complement",

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.",

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

note = "Funding Information: Acknowledgments 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.",

year = "2001",

doi = "10.1038/90686",

language = "English (US)",

volume = "2",

pages = "739--745",

journal = "Nature immunology",

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T1 - Contribution of the innate immune system to autoimmune myocarditis

T2 - A role for complement

AU - Kaya, Ziya

AU - Afanasyeva, Marina

AU - Wang, Yan

AU - Dohmen, K. Malte

AU - Schlichting, Jens

AU - Tretter, Theresa

AU - Fairweather, De Lisa

AU - Holers, V. Michael

AU - Rose, Noel R.

N1 - Funding Information: Acknowledgments 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.

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

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JF - Nature immunology

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

Abstract

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