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

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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  • 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 [156]

  • The TLR4, caspase-1, and NLRP3 pathways are upregulated in patients, EAM, autoimmune CVB3 myocarditis, and CVB3-only models and increase IL-1β and IL-18 levels in the heart.

    “Another key pathway upregulated in patients, EAM, autoimmune CVB3 myocarditis, and CVB3only models is the TLR4, caspase-1, and NLRP3 pathways that increase IL-1 β and IL-18 levels in the heart. 124,146,152,156,161-164”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [156]

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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 › Cardiology and Cardiovascular Medicine › 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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