Evidence map›Paper›PMID 23290522›Full record

ArticleImmunity2013

The kinase PKCα selectively upregulates interleukin-17A during Th17 cell immune responses.

Marlies Meisel, Natascha Hermann-Kleiter, Reinhard Hinterleitner, Thomas Gruber, Katarzyna Wachowicz, Christa Pfeifhofer-Obermair, Friedrich Fresser, Michael Leitges, Cristiana Soldani, Antonella Viola and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Lipid peroxidation of immune cells in cancer.Frontiers in immunology · 2023
    Review
  6. Inflammatory Cytokines That Enhance Antigen Responsiveness of Naïve CD8International journal of molecular sciences · 2022
    Article
  7. Article
  8. Protein Kinase C-α Is a Gatekeeper ofInfection and immunity · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Observational
  18. Loss-of-function phenotype of a PKCθCell communication and signaling : CCS · 2019
    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

12 authors at 4 institutions in 2 countries.

Marlies MeiselDepartment for Pharmacology and Genetics, Division of Translational Cell Genetics, Medical University of Innsbruck, Innsbruck 6020, Austria.
Natascha Hermann-Kleiter
Reinhard Hinterleitner
Thomas Gruber
Katarzyna Wachowicz
Christa Pfeifhofer-Obermair
Friedrich Fresser
Michael Leitges
Cristiana Soldani
Antonella Viola
Sandra Kaminski
Gottfried Baier
Innsbruck Medical University · ATUniversität Innsbruck · ATHumanitas University · ITUniversity of Milan · IT

Funding

Austrian Science Fund FWF P 23537Austrian Science Fund FWF P 23537-B13Austrian Science Fund FWF P 25044Austrian Science Fund FWF T 264Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

Transforming growth-factor β (TGFβ) has been implicated in T helper 17 (Th17) cell biology and in triggering expression of interleukin-17A (IL-17A), which is a key Th17 cell cytokine. Deregulated TGFβ receptor (TGFβR) signaling has been implicated in Th17-cell-mediated autoimmune pathogenesis. Nevertheless, the full molecular mechanisms involved in the activation of the TGFβR pathway in driving IL-17A expression remain unknown. Here, we identified protein kinase C α (PKCα) as a signaling intermediate specific to the Th17 cell subset in the activation of TGFβRI. We have shown that PKCα physically interacts and functionally cooperates with TGFβRI to promote robust SMAD2-3 activation. Furthermore, PKCα-deficient (Prkca(-/-)) cells demonstrated a defect in SMAD-dependent IL-2 suppression, as well as decreased STAT3 DNA binding within the Il17a promoter. Consistently, Prkca(-/-) cells failed to mount appropriate IL-17A, but not IL-17F, responses in vitro and were resistant to induction of Th17-cell-dependent experimental autoimmune encephalomyelitis in vivo.

Indexed as

AnimalsEncephalomyelitis, Autoimmune, ExperimentalGene Expression RegulationInterleukin-17MiceMice, KnockoutMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsProtein Kinase C-alphaReceptors, Transforming Growth Factor betaSignal TransductionSmad ProteinsSubstrate SpecificityTh17 CellsInterleukin-17Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsProtein Kinase C-alphaReceptors, Transforming Growth Factor betaSmad Proteins

Identifiers

PMID23290522
PMCPMC3556779
OpenAlexW2044133388

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.