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Cited by 150Viral Infections and Immunology ResearchCardiac Fibrosis and RemodelingOcular Diseases and Behçet’s Syndrome

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Interleukin-6–Deficient Mice Resist Development of Autoimmune Myocarditis Associated With Impaired Upregulation of Complement C3

Eriksson, Urs, Kurrer, Michael O., Schmitz, Nicole, Marsch, Stephan C., Fontana, Adriano, Eugster, Hans-Pietro, Kopf, Manfred·2003·Circulation
DOI 10.1161/01.cir.0000043802.38699.66
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Abstract

Background— Interleukin (IL)-6 regulates various aspects of the immune response. In the context of heart diseases, it has been recognized as a prognostic factor for dilated cardiomyopathy, which often results from myocarditis. Methods and Results— Using IL-6–deficient mice, we studied the role of IL-6 in a model of autoimmune myocarditis resulting from immunization with a peptide derived from cardiac α-myosin. Prevalence and severity of myocarditis were markedly reduced in the absence of IL-6. CD4 + T cells from immunized IL-6–deficient mice proliferated poorly on restimulation with specific antigen in vitro and did not mediate disease on adoptive transfer into IL-6–competent RAG-2–deficient mice, which otherwise lack B cells and T cells. Production of complement C3, a crucial factor for the development of myocarditis, was strongly upregulated in IL-6 +/+ but not in IL-6–deficient mice after immunization. Conclusions— Our results demonstrate that IL-6 is required for the expansion of autoimmune CD4 + T cells and the pathogenesis of autoimmune myocarditis, possibly by upregulation of complement C3.

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Crossref · 10.1161/01.cir.0000043802.38699.66

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  1. 10.1161/circ.95.3.655 · DOI
  2. 10.1161/circ.104.25.3145 · DOI
  3. 10.1161/circ.101.15.1767 · DOI
  4. 1998, Am J Physiol, 275, R1584
  5. 10.1161/res.86.3.281 · DOI

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Metadata

Authors
Eriksson, U., Kurrer, M. O., Schmitz, N., Marsch, S. C., Fontana, A., Eugster, H.-P., & Kopf, M.
Affiliations
  • University Hospital of Basel (CH)
  • From the Department of Internal Medicine (U.E., S.C.M.), University Hospital, Basel; Departments of Pathology (M.O.K.) and Clinical Immunology (A.F., H.-P.E.), University Hospital, Zurich; and Molecular Biomedicine (N.S., M.K.), Swiss Federal Institute of Technology, Zurich, Switzerland.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-01-21
Volume
107
Issue
2
Pages
320-325
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.0000043802.38699.66
OpenAlex
W2022616509
Cited by
150
References
32
Citations by year
2026: 6 · 2025: 5 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 5 · 2020: 9 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 9 · 2015: 9 · 2014: 6 · 2013: 11 · 2012: 13
FWCI
4.96
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Schweizerische Herzstiftung
  • Helmut Horten Stiftung
Topics
  • Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords
interleukin-6, autoimmune myocarditis, complement C3, CD4+ T cells, IL-6-deficient mice, dilated cardiomyopathy, T cell proliferation, adoptive transfer
MeSH terms
Animals, Autoantibodies, Autoimmune Diseases, B-Lymphocytes, Cell Division, Cells, Cultured, Complement C3, Disease Models, Animal, Disease Susceptibility, DNA-Binding Proteins, Immunization, Immunohistochemistry, Mice, Inbred BALB C, Myocarditis, Myocardium, Peptide Fragments, Tumor Necrosis Factor-alpha, CD4-Positive T-Lymphocytes, Interleukin-6, Up-Regulation, Mice, Knockout, Adoptive Transfer, Ventricular Myosins, Mice

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