Evidence map›Paper›PMID 24919548›Full record

ReviewCell communication and signaling : CCS2014

Orphan nuclear receptor NR2F6 acts as an essential gatekeeper of Th17 CD4+ T cell effector functions.

Natascha Hermann-Kleiter, Gottfried Baier

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2014. 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
0.5field-weighted citation impact, top 33% 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, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Inflammation and DKK1-induced AKT activation contribute to endothelial dysfunction following NR2F2 loss.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. High throughput screening for compounds to the orphan nuclear receptor NR2F6.SLAS discovery : advancing life sciences R & D · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. NR2F6 as a Prognostic Biomarker in HNSCC.International journal of molecular sciences · 2020
    Article
  14. Review
  15. Review
  16. 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

2 authors at 1 institution in 1 country.

Natascha Hermann-KleiterDepartment for Pharmacology and Genetics, Translational Cell Genetics, Medical University of Innsbruck, Peter Mayr Str, 1a, A-6020, Innsbruck, Austria. natascha.kleiter@i-med.ac.at.
Gottfried Baier
Universität Innsbruck · AT

Funding

Austrian Science Fund FWF P 23537Austrian Science Fund FWF P 23537-B13Austrian Science Fund FWF P 25044
6 · The paper itself

Abstract

Members of the evolutionarily conserved family of the chicken ovalbumin upstream promoter transcription factor NR2F/COUP-TF orphan receptors have been implicated in lymphocyte biology, ranging from activation to differentiation and elicitation of immune effector functions. In particular, a CD4+ T cell intrinsic and non-redundant function of NR2F6 as a potent and selective repressor of the transcription of the pro-inflammatory cytokines interleukin (Il) 2, interferon y (ifng) and consequently of T helper (Th)17 CD4+ T cell-mediated autoimmune disorders has been discovered. NR2F6 serves as an antigen receptor signaling threshold-regulated barrier against autoimmunity where NR2F6 is part of a negative feedback loop that limits inflammatory tissue damage induced by weakly immunogenic antigens such as self-antigens. Under such low affinity antigen receptor stimulation, NR2F6 appears as a prototypical repressor that functions to "lock out" harmful Th17 lineage effector transcription. Mechanistically, only sustained high affinity antigen receptor-induced protein kinase C (PKC)-mediated phosphorylation has been shown to inactivate NR2F6, thereby displacing pre-bound NR2F6 from the DNA and, subsequently, allowing for robust NFAT/AP-1- and RORγt-mediated cytokine transcription. The NR2F6 target gene repertoire thus identifies a general anti-inflammatory gatekeeper role for this orphan receptor. Investigating these signaling pathway(s) will enable a greater knowledge of the genetic, immune, and environmental mechanisms that lead to chronic inflammation and of certain autoimmune disorders in a given individual.

Indexed as

AnimalsAutoimmunityCOUP Transcription FactorsCytokinesHumansInflammationTh17 CellsTranscription, GeneticCOUP Transcription FactorsCytokines

Identifiers

PMID24919548
PMCPMC4066320
OpenAlexW2150899372

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.