Evidence map›Paper›PMID 28219890›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Local TNFR1 Signaling Licenses Murine Neutrophils for Increased TLR-Dependent Cytokine and Eicosanoid Production.

Jacques Deguine, Jessica Wei, Roman Barbalat, Karsten Gronert, Gregory M Barton

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. 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
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Pro-inflammatory cytokine responses toFrontiers in tropical diseases · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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

5 authors at 1 institution in 1 country.

Jacques DeguineDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720; and.
Jessica WeiVision Science Program, School of Optometry, University of California Berkeley, Berkeley, CA 94598.ORCID 0000-0002-7329-2812
Roman BarbalatDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720; and.ORCID 0000-0003-2139-913X
Karsten GronertVision Science Program, School of Optometry, University of California Berkeley, Berkeley, CA 94598.
Gregory M BartonDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720; and barton@berkeley.edu.
University of California, Berkeley · US

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STANLEY, SARAH A · 2004 to 2025
$45.5M
The cell biology of Toll-like receptor 9: a mechanism to prevent autoimmunityR01AI072429 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI Gregory M Barton · 2008 to 2026
$7.6M
Innate immunity and Salmonella pathogenesisR01AI104914 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARTON, GREGORY M · 2013 to 2017
$1.7M
Regulatory Tissue Polymorphonuclear Leukocytes Determinants of Ocular Immune ResponsesR01EY026082 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI GRONERT, KARSTEN · 2016 to 2019
$1.5M
Host-Pathogen interactions between Salmonella and Toll-like receptorsR01AI095587 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARTON, GREGORY M · 2012 to 2015
$1.5M
Sex-specific Regulation of Acute Inflammation and ResolutionR01EY022208 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI GRONERT, KARSTEN · 2012 to 2015
$1.5M
Host-Pathogen interactions between Salmonella and Toll-like receptorsR56AI095587 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARTON, GREGORY M · 2011 to 2011
$376k
NEI NIH HHS R01 EY022208NEI NIH HHS R01 EY026082NIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI072429NIAID NIH HHS R01 AI095587NIAID NIH HHS R01 AI104914NIAID NIH HHS R56 AI095587
6 · The paper itself

Abstract

Neutrophils are generally the first immune cells recruited during the development of sterile or microbial inflammation. As these cells express many innate immune receptors with the potential to directly recognize microbial or endogenous signals, we set out to assess whether their functions are locally influenced by the signals present at the onset of inflammation. Using a mouse model of peritonitis, we demonstrate that neutrophils elicited in the presence of C-type lectin receptor ligands have an increased ability to produce cytokines, chemokines, and lipid mediators in response to subsequent TLR stimulation. Importantly, we found that licensing of cytokine production was mediated by paracrine TNF-α-TNFR1 signaling rather than direct ligand sensing, suggesting a form of quorum sensing among neutrophils. Mechanistically, licensing was largely imparted by changes in the posttranscriptional regulation of inflammatory cytokines, whereas production of IL-10 was regulated at the transcriptional level. Altogether, our data suggest that neutrophils rapidly adapt their functions to the local inflammatory milieu. These phenotypic changes may promote rapid neutrophil recruitment in the presence of pathogens but limit inflammation in their absence.

Indexed as

AnimalsCytokinesDisease Models, AnimalEicosanoidsFlow CytometryMiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationNeutrophilsPeritonitisPolymerase Chain ReactionReceptors, Tumor Necrosis Factor, Type ISignal TransductionToll-Like ReceptorsCytokinesEicosanoidsReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mouseToll-Like Receptors

Identifiers

PMID28219890
PMCPMC5360520
OpenAlexW2911914147

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.