Evidence map›Paper›PMID 26555456›Full record

ArticleImmunology2016

Endogenous ligands of the aryl hydrocarbon receptor regulate lung dendritic cell function.

Thomas H Thatcher, Marc A Williams, Stephen J Pollock, Claire E McCarthy, Shannon H Lacy, Richard P Phipps, Patricia J Sime

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  4. Article
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  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Biomedicines · 2020
    Article
  15. The Aryl Hydrocarbon Receptor in Asthma: Friend or Foe?International journal of molecular sciences · 2020
    Review
  16. Article
  17. Kynurenic acid and cancer: facts and controversies.Cellular and molecular life sciences : CMLS · 2020
    Review
  18. Reimagining IDO Pathway Inhibition in Cancer Immunotherapy via Downstream Focus on the Tryptophan-Kynurenine-Aryl Hydrocarbon Axis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Review
  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

7 authors at 1 institution in 1 country.

Thomas H ThatcherDivision of Pulmonary and Critical Care Medicine, University of Rochester, Rochester, NY, USA.
Marc A WilliamsDivision of Pulmonary and Critical Care Medicine, University of Rochester, Rochester, NY, USA.
Stephen J PollockDepartment of Environmental Medicine, University of Rochester, Rochester, NY, USA.
Claire E McCarthyDepartment of Environmental Medicine, University of Rochester, Rochester, NY, USA.
Shannon H LacyDepartment of Environmental Medicine, University of Rochester, Rochester, NY, USA.
Richard P PhippsDepartment of Environmental Medicine, University of Rochester, Rochester, NY, USA.
Patricia J SimeDivision of Pulmonary and Critical Care Medicine, University of Rochester, Rochester, NY, USA.
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
The University of Rochester's Clinical and Translational Science InstituteUL1TR000042 · NCATS · UNIVERSITY OF ROCHESTER · PI BENNETT, NANCY M, KIEBURTZ, KARL D. · 2012 to 2015
$14.4M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
REGULATION OF IMMUNITY BY PROSTAGLANDINSR01DE011390 · NIDCR · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 1994 to 2009
$2.7M
Role of the Aryl Hydrocarbon Receptor in Lung InflammationR01HL088325 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2008 to 2012
$1.9M
Novel therapies for cigarette smoke induced lung injuryR01HL120908 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2014 to 2017
$1.6M
Role of cyclooxygenase-2 in antibody responses to vaccinationR21AI071064 · NIAID · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 2007 to 2008
$420k
NCATS NIH HHS UL1 TR000042NCATS NIH HHS UL1TR000042NCRR NIH HHS UL1 RR024160NCRR NIH HHS UL1RR024160NHLBI NIH HHS HL088325NHLBI NIH HHS HL120908NHLBI NIH HHS R01 HL088325NHLBI NIH HHS R01 HL120908NHLBI NIH HHS T32 HL066988NHLBI NIH HHS T32HL66988NIAID NIH HHS AI071064NIAID NIH HHS R21 AI071064NIDCR NIH HHS DE011390NIDCR NIH HHS R01 DE011390NIEHS NIH HHS P30 ES001247NIEHS NIH HHS T32 ES007026NIEHS NIH HHS T32ES01247
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a transcription factor that has been extensively studied as a regulator of toxicant metabolism. However, recent evidence indicates that the AhR also plays an important role in immunity. We hypothesized that the AhR is a novel, immune regulator of T helper type 2 (Th2) -mediated allergic airway disease. Here, we report that AhR-deficient mice develop increased allergic responses to the model allergen ovalbumin (OVA), which are driven in part by increased dendritic cell (DC) functional activation. AhR knockout (AhR(-/-) ) mice sensitized and challenged with OVA develop an increased inflammatory response in the lung compared with wild-type controls, with greater numbers of inflammatory eosinophils and neutrophils, greater T-cell proliferation, greater production of Th2 cytokines, and higher levels of OVA-specific IgE and IgG1. Lung DCs from AhR(-/-) mice stimulated antigen-specific proliferation and Th2 cytokine production by naive T cells in vitro. Additionally, AhR(-/-) DCs produced higher levels of tumour necrosis factor-α and interleukin-6, which promote Th2 differentiation, and expressed higher cell surface levels of stimulatory MHC Class II and CD86 molecules. Overall, loss of the AhR was associated with enhanced T-cell activation by pulmonary DCs and heightened pro-inflammatory allergic responses. This suggests that endogenous AhR ligands are involved in the normal regulation of Th2-mediated immunity in the lung via a DC-dependent mechanism. Therefore, the AhR may represent an important target for therapeutic intervention in allergic airways inflammation.

Indexed as

AnimalsAntigen PresentationBasic Helix-Loop-Helix ProteinsCarbazolesCell ProliferationCells, CulturedCoculture TechniquesCytokinesDendritic CellsDisease Models, AnimalImmunity, CellularImmunity, MucosalInflammation MediatorsLigandsLungLymphocyte Activation6-formylindolo(3,2-b)carbazoleAhr protein, mouseBasic Helix-Loop-Helix ProteinsCarbazolesCytokinesInflammation MediatorsLigandsOvalbuminReceptors, Aryl Hydrocarbonallergyantigen presentation/processingdendritic cellslungT helper type 1/type 2 cells

Identifiers

PMID26555456
PMCPMC4693882
OpenAlexW2122978207

What OpenQuestion holds

Textmetadata
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.