Evidence map›Paper›PMID 22539792›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Dendritic cells activated by IFN-γ/STAT1 express IL-31 receptor and release proinflammatory mediators upon IL-31 treatment.

Jutta Horejs-Hoeck, Harald Schwarz, Sebastian Lamprecht, Elisabeth Maier, Stefan Hainzl, Maria Schmittner, Gernot Posselt, Angelika Stoecklinger, Thomas Hawranek, Albert Duschl

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. IL-31: State of the Art for an Inflammation-Oriented Interleukin.International journal of molecular sciences · 2022
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. IL-31 induces antitumor immunity in breast carcinoma.Journal for immunotherapy of cancer · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Jutta Horejs-HoeckDepartment of Molecular Biology, University of Salzburg, A-5020 Salzburg, Austria. jutta.horejs_hoeck@sbg.ac.at
Harald Schwarz
Sebastian Lamprecht
Elisabeth Maier
Stefan Hainzl
Maria Schmittner
Gernot Posselt
Angelika Stoecklinger
Thomas Hawranek
Albert Duschl
University of Salzburg · ATParacelsus Medical University · AT

Funding

Austrian Science Fund FWF P 22202
6 · The paper itself

Abstract

IL-31 is a T cell-derived cytokine that signals via a heterodimeric receptor composed of IL-31Rα and oncostatin M receptor β. Although several studies have aimed to investigate IL-31-mediated effects, the biological functions of this cytokine are currently not well understood. IL-31 expression correlates with the expression of IL-4 and IL-13 and is associated with atopic dermatitis in humans, indicating that IL-31 is involved in Th2-mediated skin inflammation. Because dendritic cells are the main activators of Th cell responses, we posed the question of whether dendritic cells express the IL-31R complex and govern immune responses triggered by IL-31. In the current study, we report that primary human CD1c(+) as well as monocyte-derived dendritic cells significantly upregulate the IL-31Rα receptor chain upon stimulation with IFN-γ. EMSAs, chromatin immunoprecipitation assays, and small interfering RNA-based silencing assays revealed that STAT1 is the main transcription factor involved in IFN-γ-dependent IL-31Rα expression. Subsequent IL-31 stimulation resulted in a dose-dependent release of proinflammatory mediators, including TNF-α, IL-6, CXCL8, CCL2, CCL5, and CCL22. Because these cytokines are crucially involved in skin inflammation, we hypothesize that IL-31-specific activation of dendritic cells may be part of a positive feedback loop driving the progression of inflammatory skin diseases.

Indexed as

Cells, CulturedDendritic CellsFeedbackHumansInflammationInflammation MediatorsInterferon-gammaReceptors, InterleukinSkin DiseasesSTAT1 Transcription FactorIL31RA protein, humanInflammation MediatorsInterferon-gammaReceptors, InterleukinSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID22539792
PMCPMC4766741
OpenAlexW2129750783

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.