Evidence map›Paper›PMID 25203682›Full record

ArticlePloS one2014

The aryl hydrocarbon receptor: differential contribution to T helper 17 and T cytotoxic 17 cell development.

Mark D Hayes, Vitalijs Ovcinnikovs, Andrew G Smith, Ian Kimber, Rebecca J Dearman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Impact of cardiac resynchronization therapy on circulating IL-17 producing cells in patients with advanced heart failure.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2019
    Article
  6. Article
  7. Laquinimod arrests experimental autoimmune encephalomyelitis by activating the aryl hydrocarbon receptor.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  8. Article
  9. Review
  10. New Trends in Aryl Hydrocarbon Receptor Biology.Frontiers in cell and developmental biology · 2016
    Review
  11. Article
  12. Article
  13. 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

5 authors at 2 institutions in 1 country.

Mark D HayesFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
Vitalijs OvcinnikovsFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
Andrew G SmithMRC Toxicology Unit, The University of Leicester, Leicester, United Kingdom.
Ian KimberFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
Rebecca J DearmanFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
University of Manchester · GBUniversity of Leicester · GB

Funding

Medical Research Council MR/J500410/1
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) has been shown to be required for optimal Thelper (Th) 17 cell activation. Th17 cells provide immunity against extracellular pathogens and are implicated in autoimmune diseases. Herein, the role of the AhR in cytokine production by Th17, and by the analogous population of T cytotoxic (Tc)17 cells, has been examined. Lymph node Tc (CD8(+)) and Th (CD4(+)) cells were isolated by negative selection from naive AhR(+/-) and AhR(-/-) mice and polarised to Tc1/Th1 or Tc17/Th17 phenotypes with appropriate cytokines. Cell differentiation was assessed as a function of mRNA and protein (ELISA and flow cytometry) expression for interferon (IFN)-γ and for key Th17 cytokines. In AhR(+/-) mice, Th17 cells displayed an exclusive IL-17 profile, which was markedly inhibited by a selective AhR antagonist to levels observed in AhR knockout mice. Addition of the natural AhR agonist 6-formylindolo[3,2-b]carbazole (FICZ) markedly enhanced Th17 cell activity in the heterozygotes. In contrast, Tc17 cells polarised into 3 distinct subsets: producing either IL-17 or IFN-γ alone, or both cytokines. Blocking AhR was also detrimental to Tc17 development, with reduced responses recorded in AhR(-/-) mice and antagonist-mediated reduction of IL-17 expression in the heterozygotes. However, Tc17 cells were largely refractory to exogenous FICZ, presumably because Tc17 cells express baseline AhR mRNA, but unlike Th17 cells, there is no marked up-regulation during polarisation. Thus, Th17 cell development is more dependent upon AhR activation than is Tc17 cell development, suggesting that endogenous AhR ligands play a much greater role in driving Th17 cell responses.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsFemaleGene Expression RegulationGene Knockout TechniquesInterleukin-17Interleukin-22InterleukinsKineticsMaleMiceReceptors, Aryl HydrocarbonRNA, MessengerTh17 CellsT-Lymphocytes, CytotoxicAhr protein, mouseBasic Helix-Loop-Helix ProteinsInterleukin-17Interleukin-22InterleukinsReceptors, Aryl HydrocarbonRNA, Messenger

Identifiers

PMID25203682
PMCPMC4159274
OpenAlexW2046580414

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.