Evidence map›Paper›PMID 25716673›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2015

Differential regulation of Th17 and T regulatory cell differentiation by aryl hydrocarbon receptor dependent xenobiotic response element dependent and independent pathways.

Sonia Mohinta, Arun K Kannan, Krishne Gowda, Shantu G Amin, Gary H Perdew, Avery August

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

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  18. The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health.International journal of molecular sciences · 2018
    Review
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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

6 authors at 1 institution in 1 country.

Sonia Mohinta*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801.
Arun K Kannan*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801.
Krishne Gowda*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801.
Shantu G Amin*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801.
Gary H Perdew*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801.
Avery August*Department of Microbiology and Immunology, Cornell University, Ithaca, New York 14853, Department of Pharmacology, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033 and Center for Molecular Toxicology, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16801 averyaugust@cornell.edu.
Pennsylvania State University · US

Funding

REGULATION OF THE AH RECEPTORR01ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H. · 1994 to 2017
$5.3M
Tyrosine Kinase ITK in Experimental Allergic AsthmaR01AI051626 · NIAID · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI AUGUST, AVERY · 2003 to 2012
$3.6M
Selective Ah Receptor Ligands Repress Acute-Phase ResponseR01ES019964 · NIEHS · PENNSYLVANIA STATE UNIVERSITY, THE · PI PERDEW, GARY H. · 2012 to 2016
$2.0M
Eosinophils and Allergic Airway ResponsesR01AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2012
$1.9M
Selective Aryl Hydrocarbon Receptor Modulators and T cell Effector FunctionR21AI108958 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2014 to 2015
$430k
Eosinophils and Allergic Airway ResponsesR56AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2008
$61k
NIAID NIH HHS AI073955NIAID NIH HHS AI108958NIAID NIH HHS AI51626NIAID NIH HHS R01 AI051626NIAID NIH HHS R01 AI073955NIAID NIH HHS R21 AI108958NIEHS NIH HHS ES019964NIEHS NIH HHS R01 ES004869NIEHS NIH HHS R01 ES019964
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is regarded as an environmental sensor and has been shown to link environmental stresses with chronic inflammatory and autoimmune diseases. The AHR can be activated to regulate both the X/DRE (xenobiotic or dioxin response elements) as well as a non-X/DRE mediated pathway. Selective AHR modulators (SAhRMs) are recently identified compounds that activate non-X/DRE mediated pathway without activating the X/DRE-driven responses. Here, we have used 3 classes of AHR ligands; agonist, antagonist, and a SAhRM, to delineate the role of these AHR-driven pathways in T helper 17 (Th17)/T regulatory (Treg) regulation. We show that Th17 differentiation is primarily dependent on X/DRE-driven responses, whereas Treg differentiation can be suppressed by inhibiting non-X/DRE pathway. Using a model of Citrobacter rodentium infection, we further show that AHR agonist enhances Th17 production and promoted resolution of infection, whereas a SAhRM inhibited Th17 mediated responses with reduced resolution of infection. These data indicate that Th17/Treg function may be differentially regulated by SAhRMs that differentially activate the X/DRE and non-X/DRE mediated pathways, and point to a therapeutic strategy to leverage AHR function in the treatment of chronic inflammatory and autoimmune disease.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCells, CulturedCitrobacter rodentiumDisease Models, AnimalEnterobacteriaceae InfectionsGene Expression RegulationInterleukin-17LigandsLymphocyte ActivationMice, Inbred C57BLMice, KnockoutReceptors, Aryl HydrocarbonResponse ElementsSignal TransductionAhr protein, mouseBasic Helix-Loop-Helix ProteinsIl17a protein, mouseInterleukin-17LigandsReceptors, Aryl HydrocarbonAHRSAhRMsTh17Treg

Identifiers

PMID25716673
PMCPMC4471441
OpenAlexW2097926997

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.