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 1 (CR1) and type 2 (CR2). We also found a subset of CD44(hi)CD62L(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.
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Mice with EAM or autoimmune CVB3 myocarditis upregulate complement components during innate immune response and acute myocarditis including C3, CD11b, C3aR, and C5aR.
“Mice with experimental autoimmune myocarditis (EAM) or autoimmune CVB3 myocarditis also upregulate complement components during the innate immune response and acute myocarditis including C3, CD11b (also known as CR [complement receptor] 3), C3aR, and C5aR. 155-157”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [155]
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References 52 · Cited by 175
- Authors
- Kaya, Z., Afanasyeva, M., Wang, Y., Dohmen, K. M., Schlichting, J., Tretter, T., Fairweather, D., Holers, V. M., & Rose, N. R.
- Affiliations
- Johns Hopkins University (US)
- University of Colorado Health (US)
- Corresponding author
- Rose, Noel R.
- Venue
- Nature Immunology
- Published
- 2001-08
- Volume
- 2
- Issue
- 8
- Pages
- 739-745
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W1500257692
- Cited by
- 175
- References
- 52
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 1 · 2023: 6 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 7 · 2016: 4 · 2015: 5 · 2014: 8 · 2013: 8 · 2012: 5
- FWCI
- 8.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r21hl065100-01)
- National Heart, Lung, and Blood Institute (HL-33878, R01HL033878, HL65100)
- National Institute of Allergy and Infectious Diseases (AI31105, R01AI031105)
- National Institute of Environmental Health Sciences (ES 07141)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- autoimmune myocarditis, complement system, complement receptor 1, CR2, innate immunity, dilated cardiomyopathy, heart failure, CD44, L-selectin, T cell activation, B cell activation, T cell proliferation, cytokine production, experimental autoimmune myocarditis
- MeSH terms
- Adult, Animals, Complement System Proteins, Complement Activation, Female, Humans, Lymphocyte Activation, Myocarditis, Receptors, Complement, T-Lymphocytes, Autoimmunity, Mice
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