Evidence map›Paper›PMID 29847790›Full record

ArticleCell reports2018

A Batf3/Nlrp3/IL-18 Axis Promotes Natural Killer Cell IL-10 Production during Listeria monocytogenes Infection.

Sarah E Clark, Rebecca L Schmidt, Daniel S McDermott, Laurel L Lenz

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
  6. NLRP3 inhibition improves maternal hypertension, inflammation, and vascular dysfunction in response to placental ischemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  7. Article
  8. Review
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  11. Article
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  15. Frontiers in cell and developmental biology · 2021
    Article
  16. IL-10-producing NK cells exacerbate sublethal Streptococcus pneumoniae infection in the lung.Translational research : the journal of laboratory and clinical medicine · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Sarah E ClarkDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Rebecca L SchmidtDepartment of Biomedical Research, National Jewish Health, Denver, CO 80206, USA.
Daniel S McDermottDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Laurel L LenzDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA; Department of Biomedical Research, National Jewish Health, Denver, CO 80206, USA. Electronic address: laurel.lenz@ucdenver.edu.
University of Colorado Denver · US

Funding

Immune Modulation by Bacterial AutolysinsR01AI065638 · NIAID · UNIVERSITY OF COLORADO DENVER · PI LENZ, LAUREL L · 2006 to 2016
$3.8M
NK cell IL-10 production during bacterial infectionsR01AI131662 · NIAID · UNIVERSITY OF COLORADO DENVER · PI LENZ, LAUREL L · 2017 to 2021
$2.9M
Active Subversion of Innate Immunity by Bacterial LysM ProteinR56AI065638 · NIAID · NATIONAL JEWISH HEALTH · PI LENZ, LAUREL L · 2011 to 2011
$396k
Natural killer cell-derived IL-10 and immunity to ListeriaF32AI114075 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CLARK, SARAH E · 2014 to 2016
$164k
NIAID NIH HHS F32 AI114075NIAID NIH HHS R01 AI065638NIAID NIH HHS R01 AI131662NIAID NIH HHS R56 AI065638
6 · The paper itself

Abstract

The bacterial pathogen Listeria monocytogenes (Lm) capitalizes on natural killer (NK) cell production of regulatory interleukin (IL)-10 to establish severe systemic infections. Here, we identify regulators of this IL-10 secretion. We show that IL-18 signals to NK cells license their ability to produce IL-10. IL-18 acts independent of IL-12 and STAT4, which co-stimulate IFNγ secretion. Dendritic cell (DC) expression of Nlrp3 is required for IL-18 release in response to the Lm p60 virulence protein. Therefore, mice lacking Nlrp3, Il18, or Il18R fail to accumulate serum IL-10 and are highly resistant to systemic Lm infection. We further show that cells expressing or dependent on Batf3 are required for IL-18-inducing IL-10 production observed in infected mice. These findings explain how Il18 and Batf3 promote susceptibility to bacterial infection and demonstrate the ability of Lm to exploit NLRP3 for the promotion of regulatory NK cell activity.

Indexed as

AnimalsBacterial ProteinsBasic-Leucine Zipper Transcription FactorsDendritic CellsDisease SusceptibilityFemaleInterleukin-10Interleukin-18Interleukin-2Killer Cells, NaturalLipopolysaccharidesListeria monocytogenesListeriosisMaleMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 Protein60 kDa protein, Listeria monocytogenesBacterial ProteinsBasic-Leucine Zipper Transcription FactorsInterleukin-10Interleukin-18Interleukin-2LipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinRepressor ProteinsSNFT protein, mouseSTAT4 Transcription FactorBatf3dendritic cellimmune regulationinfectioninnate immunityinterleukin-10interleukin-18Listeria monocytogenesNatural killer cellNlrp3

Identifiers

PMID29847790
PMCPMC6170157
OpenAlexW2805947951

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.