Evidence map›Paper›PMID 35295139›Full record

ArticleFrontiers in toxicology2021

Aryl Hydrocarbon Receptor Signaling Synergizes with TLR/NF-κB-Signaling for Induction of IL-22 Through Canonical and Non-Canonical AhR Pathways.

Yasuhiro Ishihara, Sarah Y Kado, Keith J Bein, Yi He, Arshia A Pouraryan, Angelika Urban, Thomas Haarmann-Stemmann, Colleen Sweeney, Christoph F A Vogel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in toxicology, 2021. 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
2.3field-weighted citation impact, top 11% 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, 29 citations in OpenAlex.

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  12. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  13. Article
  14. Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Review
  15. Article
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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

9 authors at 2 institutions in 3 countries.

Yasuhiro IshiharaCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Sarah Y KadoCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Keith J BeinCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Yi HeCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Arshia A PouraryanCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Angelika UrbanCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
Thomas Haarmann-StemmannLeibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.
Colleen SweeneyDepartment of Biochemistry and Molecular Medicine, School of Medicine, University of California, Davis, Davis, CA, United States.
Christoph F A VogelCenter for Health and the Environment, University of California, Davis, Davis, CA, United States.
University of California, Davis · USLeibniz Institute of Environmental Medicine · DE

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
Air pollution, atherosclerosis, and the role of the aryl hydrocarbon receptorR01ES029126 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2023
$1.8M
The impact of Aryl hydrocarbon receptor signaling on Toll like receptor-mediated inflammationR01ES032827 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHRISTOPH F A VOGEL · 2022 to 2026
$1.7M
The protective role of the AhR Repressor in breast cancer developmentR21ES030419 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2020
$432k
NIEHS NIH HHS P30 ES023513NIEHS NIH HHS R01 ES029126NIEHS NIH HHS R01 ES032827NIEHS NIH HHS R21 ES030419
6 · The paper itself

Abstract

Interleukin 22 (IL-22) is critically involved in gut immunity and host defense and primarily produced by activated T cells. In different circumstances IL-22 may contribute to pathological conditions or act as a cancer promoting cytokine secreted by infiltrating immune cells. Here we show that bone marrow-derived macrophages (BMM) express and produce IL-22 after activation of the aryl hydrocarbon receptor (AhR) when cells are activated through the Toll-like receptor (TLR) family. The additional activation of AhR triggered a significant induction of IL-22 in TLR-activated BMM. Deletion and mutation constructs of the IL-22 promoter revealed that a consensus DRE and RelBAhRE binding element are necessary to mediate the synergistic effects of AhR and TLR ligands. Inhibitor studies and analysis of BMM derived from knockout mice confirmed that the synergistic induction of IL-22 by AhR and TLR ligands depend on the expression of AhR and Nuclear Factor-kappa B (NF-κB) member RelB. The exposure to particulate matter (PM) collected from traffic related air pollution (TRAP) and wildfires activated AhR as well as NF-κB signaling and significantly induced the expression of IL-22. In summary this study shows that simultaneous activation of the AhR and NF-κB signaling pathways leads to synergistic and prolonged induction of IL-22 by integrating signals of the canonical and non-canonical AhR pathway.

Indexed as

AhRIL-22inflammationmacrophagestoll-like receptor

Identifiers

PMID35295139
PMCPMC8915841
OpenAlexW4210408121

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.