Evidence map›Paper›PMID 25622543›Full record

ArticleThe American journal of pathology2015

Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration.

SuFey Ong, Davinna L Ligons, Jobert G Barin, Lei Wu, Monica V Talor, Nicola Diny, Jillian A Fontes, Elizabeth Gebremariam, David A Kass, Noel R Rose and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Unconventional functions of natural killer cells in homeostasis and disease.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  6. Article
  7. Integrating mechanical cues inFrontiers in immunology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Immunology of human fibrosis.Nature immunology · 2023
    Review
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

SuFey OngThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland.
Davinna L LigonsDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jobert G BarinDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lei WuThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland.
Monica V TalorDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Nicola DinyThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland.
Jillian A FontesThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland.
Elizabeth GebremariamDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
David A KassDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Noel R RoseThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Daniela ČihákováThe W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address: dcihako1@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Myeloid Cells are Critical in Inflammatory Heart DiseaseR01HL118183 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2014 to 2023
$4.4M
Eosinophilic MyocarditisR01HL113008 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2012 to 2015
$1.6M
Role of Natural Killer Cells in Myocarditis and Dilated CardiomyopathyF31HL112665 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ONG, SUFEY · 2012 to 2013
$84k
NHLBI NIH HHS F31 HL112665NHLBI NIH HHS F31 HL112665-01A1NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R01HL113008NHLBI NIH HHS R01 HL118183NHLBI NIH HHS R01HL118183
6 · The paper itself

Abstract

Myocarditis is a leading cause of sudden cardiac failure in young adults. Natural killer (NK) cells, a subset of the innate lymphoid cell compartment, are protective in viral myocarditis. Herein, we demonstrated that these protective qualities extend to suppressing autoimmune inflammation. Experimental autoimmune myocarditis (EAM) was initiated in BALB/c mice by immunization with myocarditogenic peptide. During EAM, activated cardiac NK cells secreted interferon γ, perforin, and granzyme B, and expressed CD69, tumor necrosis factor-related apoptosis-inducing ligand treatment, and CD27 on their cell surfaces. The depletion of NK cells during EAM with anti-asialo GM1 antibody significantly increased myocarditis severity, and was accompanied by elevated fibrosis and a 10-fold increase in the percentage of cardiac-infiltrating eosinophils. The resultant influx of eosinophils to the heart was directly responsible for the increased disease severity in the absence of NK cells, because treatment with polyclonal antibody asialogangloside GM-1 did not augment myocarditis severity in eosinophil-deficient ΔdoubleGATA1 mice. We demonstrate that NK cells limit eosinophilic infiltration both indirectly, through altering eosinophil-related chemokine production by cardiac fibroblasts, and directly, by inducing eosinophil apoptosis in vitro. Altogether, we define a new pathway of eosinophilic regulation through interactions with NK cells.

Indexed as

AnimalsApoptosisEosinophilsFibrosisInflammationKiller Cells, NaturalMiceMice, Inbred BALB CMyocarditisMyocardium

Identifiers

PMID25622543
PMCPMC4348473
OpenAlexW2163656392

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.