CoChat
Sign Up
Cited by 158Viral Infections and Immunology ResearchImmunotherapy and Immune ResponsesT-cell and B-cell Immunology

Activation of Dendritic Cells through the Interleukin 1 Receptor 1 Is Critical for the Induction of Autoimmune Myocarditis

Open access
Eriksson, Urs, Kurrer, Michael O., Sonderegger, Ivo, Iezzi, Giandomenica, Tafuri, Anna, Hunziker, Lukas, Suzuki, Shinobu, Bachmaier, Kurt +3 more·2003·The Journal of Experimental Medicine
DOI 10.1084/jem.20021788PMC PMC2193833
Open this paper in CoChat — free accountOpen PDF

Abstract

Dilated cardiomyopathy, resulting from myocarditis, is the most common cause of heart failure in young patients. We here show that interleukin (IL)-1 receptor type 1–deficient (IL-1R1−/−) mice are protected from development of autoimmune myocarditis after immunization with α-myosin-peptide(614–629). CD4+ T cells from immunized IL-1R1−/− mice proliferated poorly and failed to transfer disease after injection into naive severe combined immunodeficiency (SCID) mice. In vitro stimulation experiments suggested that the function of IL-1R1−/−CD4+ T cells was not intrinsically defect, but their activation by dendritic cells was impaired in IL-1R1−/− mice. Accordingly, production of tumor necrosis factor (TNF)-α, IL-1, IL-6, and IL-12p70 was reduced in dendritic cells lacking the IL-1 receptor type 1. In fact, injection of immature, antigen-loaded IL-1R1+/+ but not IL-1R1−/− dendritic cells into IL-1R1−/− mice fully restored disease susceptibility by rendering IL-1R1−/− CD4+ T cells pathogenic. Thus, IL-1R1 triggering is required for efficient activation of dendritic cells, which is in turn a prerequisite for induction of autoreactive CD4+ T cells and autoimmunity.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1084/jem.20021788

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • IL-1β increases serum and cardiac IL-6 levels that are needed to drive Th17 responses, which promote fibrosis and progression to DCM and heart failure in patients with myocarditis and in animal models.

    “IL-1 β also increases serum and cardiac IL-6 levels that are needed to drive Th17 responses, which also promote fibrosis and progression to DCM and heart failure in patients with myocarditis and in animal models. 36,165,172-174”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [165]

    The Results and Discussion (page unavailable) show that IL-1R1 signaling and IL-1β contribute to IL-6 production by stimulated mouse dendritic cells, and the Introduction links myocarditis with cardiomyopathy and heart failure. The paper does not show increased serum or cardiac IL-6, establish a Th17 response or fibrosis pathway, or test that proposed progression in patients. (LLM, conf=0.89)

    Experimental — accuracy not yet measured

  • IL-18 strongly drives Th1 immune responses, but in BALB/c mice, this produces a mixed Th1/Th2 response that promotes fibrosis and DCM rather than a classical STAT-driven Th1 response.

    “IL-18, originally named IFNγ -inducing factor, strongly drives Th1 immune responses, 143-145 but in BALB/c mice, this produces a mixed Th1/Th2 response that promotes fibrosis and DCM rather than a classical STAT-driven Th1 respo nse. 115,146,160,165”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [165]

    The Discussion mentions IL-18 in a signaling pathway and separately discusses Th1 and Th2 responses, but does not describe an IL-18-induced mixed Th1/Th2 response in BALB/c mice. The BALB/c Results examine IL-1R1-dependent myocarditis; searches for fibrosis, DCM, and STAT did not establish the claimed IL-18-driven outcome. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Eriksson, U., Kurrer, M. O., Sonderegger, I., Iezzi, G., Tafuri, A., Hunziker, L., Suzuki, S., Bachmaier, K., Bingisser, R. M., Penninger, J. M., & Kopf, M.
Affiliations
  • University Health Network (CA)
  • University Hospital Zurich (CH)
  • ETH Zurich (CH)
  • University Hospital of Basel (CH)
  • Institute of Molecular Biotechnology (AT)
  • 5Molecular Biomedicine, Swiss Federal Institute of Technology, CH-8952 Zurich, Switzerland
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2003-01-27
Volume
197
Issue
3
Pages
323-331
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.20021788
PMC
PMC2193833
OpenAlex
W2129077500
Cited by
158
References
43
Citations by year
2026: 1 · 2025: 3 · 2024: 5 · 2023: 6 · 2022: 3 · 2021: 6 · 2020: 5 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 8 · 2015: 2 · 2014: 4 · 2013: 8 · 2012: 6
FWCI
11.02
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • Novartis Foundation
  • Schweizerische Herzstiftung
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
IL1R1, dendritic cell activation, autoimmune myocarditis, dilated cardiomyopathy, CD4+ T cell activation, autoreactive T cells, heart failure
MeSH terms
Amino Acid Sequence, Animals, Autoimmune Diseases, Cardiomyopathy, Dilated, Dendritic Cells, Female, Humans, Mice, Inbred BALB C, Molecular Sequence Data, Myocarditis, Peptide Fragments, CD4-Positive T-Lymphocytes, Autoimmunity, Cytokines, Mice, SCID, Receptors, Interleukin-1, Mice, Knockout, Adoptive Transfer, Ventricular Myosins, Mice, Receptors, Interleukin-1 Type I

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review