Evidence map›Paper›PMID 27621211›Full record

ArticleEuropean journal of immunology2016

Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart.

Nicola L Diny, Xuezhou Hou, Jobert G Barin, Guobao Chen, Monica V Talor, Julie Schaub, Stuart D Russell, Karin Klingel, Noel R Rose, Daniela Čiháková

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

  1. Tissue adaptation of eosinophils.Journal of leukocyte biology · 2026
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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

10 authors at 2 institutions in 2 countries.

Nicola L DinyW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Xuezhou HouW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Jobert G BarinDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Guobao ChenDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Monica V TalorDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Julie SchaubDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Stuart D RussellDepartment of Medicine Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Karin KlingelAbteilung für Molekulare Pathologie, Eberhard Karls Universität Tübingen, Tübingen, Germany.
Noel R RoseW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Daniela ČihákováW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Johns Hopkins University · USUniversity of Tübingen · DE

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
NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R01 HL118183
6 · The paper itself

Abstract

Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in which experimental autoimmune myocarditis (EAM) is induced in IFNγ

Indexed as

AdultAgedAnimalsCardiac MyosinsCell MovementCells, CulturedChemokine CCL11Chemokine CCL24EosinophilsFemaleFibroblastsHumansInterferon-gammaMacrophagesMaleMiceCardiac MyosinsCcl11 protein, mouseCcl24 protein, mouseCcr3 protein, mouseChemokine CCL11Chemokine CCL24Interferon-gammaReceptors, CCR3CardiomyopathyCell traffickingChemokinesEosinophilsEotaxinsExperimental autoimmune myocarditisInflammation

Identifiers

PMID27621211
PMCPMC5404278
OpenAlexW2519720623

What OpenQuestion holds

Textmetadata
LicenceTDM
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.