Evidence map›Paper›PMID 39513273›Full record

ArticleCirculation. Heart failure2024

IL1RAP Blockade With a Monoclonal Antibody Reduces Cardiac Inflammation and Preserves Heart Function in Viral and Autoimmune Myocarditis.

Diego A Lema, Gabriel Jakobsson, Abdel Daoud, David Elias, Monica V Talor, Sara Rattik, Caitríona Grönberg, Hannah Kalinoski, Elin Jaensson Gyllenbäck, Nadan Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Heart failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Observational
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Giant Cell Myocarditis: Is It Time to Redeploy Cytokine Inhibitors?Mediterranean journal of rheumatology · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Diego A Lema *Department of Pathology, School of Medicine (D.A.L., D.E., M.V.T., D.Č.), Johns Hopkins University, Baltimore, MD.ORCID 0000-0001-7910-1127
Gabriel Jakobsson *Department of Translational Medicine, Lund University, Malmö, Sweden (G.J., A.S.).ORCID 0000-0001-5071-9505
Abdel DaoudW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health (A.D., H.K., D.Č.), Johns Hopkins University, Baltimore, MD.ORCID 0009-0004-6661-5670
David EliasDepartment of Pathology, School of Medicine (D.A.L., D.E., M.V.T., D.Č.), Johns Hopkins University, Baltimore, MD.ORCID 0000-0002-4363-3057
Monica V TalorDepartment of Pathology, School of Medicine (D.A.L., D.E., M.V.T., D.Č.), Johns Hopkins University, Baltimore, MD.ORCID 0000-0002-8275-5698
Sara RattikCantargia AB, Lund, Sweden (S.R., C.G., E.J.G., D.L.).
Caitríona GrönbergCantargia AB, Lund, Sweden (S.R., C.G., E.J.G., D.L.).ORCID 0009-0000-3776-5566
Hannah KalinoskiW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health (A.D., H.K., D.Č.), Johns Hopkins University, Baltimore, MD.
Elin Jaensson GyllenbäckCantargia AB, Lund, Sweden (S.R., C.G., E.J.G., D.L.).ORCID 0000-0002-1334-8642
Nadan WangDepartment of Cardiology, School of Medicine (N.W.), Johns Hopkins University, Baltimore, MD.ORCID 0000-0002-1682-080X
David LibergCantargia AB, Lund, Sweden (S.R., C.G., E.J.G., D.L.).ORCID 0009-0009-0645-746X
Alexandru Schiopu *Department of Translational Medicine, Lund University, Malmö, Sweden (G.J., A.S.).ORCID 0000-0002-7587-5050
Daniela Čiháková *Department of Pathology, School of Medicine (D.A.L., D.E., M.V.T., D.Č.), Johns Hopkins University, Baltimore, MD.ORCID 0000-0002-8713-2860

Funding

Medical Scientist Training ProgramT32GM136577 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ANDREA L COX · 2020 to 2026
$13.4M
NIGMS NIH HHS T32 GM136577
6 · The paper itself

Abstract

backgroundCurrently, there are no therapies targeting specific pathogenic pathways in myocarditis. IL (interleukin)-1 blockade has shown promise in preclinical studies and case reports. We hypothesized that blockade of IL1RAP (IL-1 receptor accessory protein), a shared subunit of the IL-1, IL-33, and IL-36 receptors, could be more efficient than IL-1 blockade alone.

methodsWe induced coxsackievirus B3 (CVB3)-mediated or experimental autoimmune myocarditis (EAM) in BALB/c mice, followed by treatment with an Fc (fragment crystallizable)-modified mIgG2a mouse anti-mouse IL1RAP monoclonal antibody (mCAN10). Myocarditis severity and immune infiltration were assessed by histology and flow cytometry. Cardiac function was measured by echocardiography. We used spatial transcriptomics (Visium 10× Genomics) to compare the gene expression landscape in the hearts of mCAN10-treated versus control mice.

resultsIL1RAP blockade reduced CVB3 and EAM severity. In EAM, the treatment prevented deterioration of cardiac function, measured on day 42 post-disease induction (left ventricular ejection fraction: 56.5% versus 51.0% in isotype controls [

conclusionsBlocking IL1RAP reduces acute CVB3 myocarditis and EAM severity and preserves cardiac function in EAM. We conclude that IL1RAP blockade is a potential therapeutic strategy in viral and autoimmune myocarditis.

Indexed as

Antibodies, MonoclonalAutoimmune DiseasesCoxsackievirus InfectionsDisease Models, AnimalInterleukin-1 Receptor Accessory ProteinMice, Inbred BALB CMyocarditisAnimalsEnterovirus B, HumanMaleMiceMyocardiumVentricular Function, LeftAntibodies, MonoclonalInterleukin-1 Receptor Accessory Proteineosinophilsflow cytometrymonocytesmyocarditistherapeutics

Identifiers

PMID39513273
PMCPMC11643131

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.