Evidence map›Paper›PMID 28432285›Full record

ArticleScientific reports2017

NOD1 modulates IL-10 signalling in human dendritic cells.

Theresa Neuper, Kornelia Ellwanger, Harald Schwarz, Thomas A Kufer, Albert Duschl, Jutta Horejs-Hoeck

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Immune network · 2019
    Article
  9. IL-1β Induces SOCS2 Expression in Human Dendritic Cells.International journal of molecular sciences · 2019
    Article
  10. Article
  11. Yangyin Qingre Huoxue Method in Traditional Chinese Medicine Ameliorates Atherosclerosis in ApoEEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  12. Article
  13. Article
  14. 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

6 authors at 2 institutions in 2 countries.

Theresa NeuperDepartment of Molecular Biology, University of Salzburg, Salzburg, Austria.
Kornelia EllwangerInstitute of Nutritional Medicine, Department of Immunology, University of Hohenheim, Stuttgart, Germany.
Harald SchwarzDepartment of Molecular Biology, University of Salzburg, Salzburg, Austria.
Thomas A KuferInstitute of Nutritional Medicine, Department of Immunology, University of Hohenheim, Stuttgart, Germany.ORCID http://orcid.org/0000-0003-4563-0412
Albert DuschlDepartment of Molecular Biology, University of Salzburg, Salzburg, Austria.ORCID http://orcid.org/0000-0002-7034-9860
Jutta Horejs-HoeckDepartment of Molecular Biology, University of Salzburg, Salzburg, Austria. jutta.horejs_hoeck@sbg.ac.at.ORCID http://orcid.org/0000-0002-0984-204X
University of Salzburg · ATUniversity of Hohenheim · DE

Funding

MOLECULAR ANALYSIS OF NEUTROPHIL ACTIVATION BY CHEMOATTRACTANTSZ01AI000615 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MURPHY, PHILIP · 1991 to 2008
$7.1M
Austrian Science Fund FWF P 29941Intramural NIH HHS Z01 AI000615
6 · The paper itself

Abstract

NOD1 belongs to the family of NOD-like receptors, which is a group of well-characterised, cytosolic pattern-recognition receptors. The best-studied function of NOD-like receptors is their role in generating immediate pro-inflammatory and antimicrobial responses by detecting specific bacterial peptidoglycans or by responding to cellular stress and danger-associated molecules. The present study describes a regulatory, peptidoglycan-independent function of NOD1 in anti-inflammatory immune responses. We report that, in human dendritic cells, NOD1 balances IL-10-induced STAT1 and STAT3 activation by a SOCS2-dependent mechanism, thereby suppressing the tolerogenic dendritic cell phenotype. Based on these findings, we propose that NOD1 contributes to inflammation not only by promoting pro-inflammatory processes, but also by suppressing anti-inflammatory pathways.

Indexed as

AnimalsCells, CulturedDendritic CellsGene SilencingHEK293 CellsHumansInterleukin-10Nod1 Signaling Adaptor ProteinPeptidoglycanPhenotypeSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorSuppressor of Cytokine Signaling ProteinsIL10 protein, humanInterleukin-10NOD1 protein, humanNod1 Signaling Adaptor ProteinPeptidoglycanSOCS2 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling Proteins

Identifiers

PMID28432285
PMCPMC5430717
OpenAlexW2606775448

What OpenQuestion holds

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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.