Evidence map›Paper›PMID 38603630›Full record

ReviewToxicological sciences : an official journal of the Society of Toxicology2024

Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.

Keegan Malany, Xiaohan Li, Christoph F A Vogel, Allison K Ehrlich

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological sciences : an official journal of the Society of Toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.6field-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

8 citing papers in PubMed, 15 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Keegan MalanyDepartment of Environmental Toxicology, University of California, Davis, California, USA.
Xiaohan LiCenter for Health and the Environment, University of California, Davis, California, USA.ORCID 0009-0003-7761-8570
Christoph F A VogelDepartment of Environmental Toxicology, University of California, Davis, California, USA.ORCID 0000-0002-7561-4598
Allison K EhrlichDepartment of Environmental Toxicology, University of California, Davis, California, USA.ORCID 0000-0002-0994-6471
University of California, Davis · US

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
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
Ah-Receptor as a central mediator of immunomodulation in the tumor microenvironment of breast cancerR01ES036338 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI COLLEEN Ann SWEENEY, CHRISTOPH F A VOGEL · 2025 to 2026
$997k
AhR activation and susceptibility to type 1 diabetesR00DK117509 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI EHRLICH, ALLISON · 2020 to 2022
$747k
NIDDK NIH HHS R00 DK117509NIDDK NIH HHS R00DK117509NIEHS NIH HHS P30 ES023513NIEHS NIH HHS R01 ES029126NIEHS NIH HHS R01 ES032827NIEHS NIH HHS R01ES032827NIEHS NIH HHS R01 ES036338NIEHS NIH HHS T32 ES007059NIH HHSUniversity of California Davis
6 · The paper itself

Abstract

Macrophages play an essential role in the innate immune system by differentiating into functionally diverse subsets in order to fight infection, repair damaged tissues, and regulate inappropriate immune responses. This functional diversity stems from their ability to adapt and respond to signals in the environment, which is in part mediated through aryl hydrocarbon receptor (AHR)-signaling. AHR, an environmental sensor, can be activated by various ligands, ranging from environmental contaminants to microbially derived tryptophan metabolites. This review discusses what is currently known about how AHR-signaling influences macrophage differentiation, polarization, and function. By discussing studies that are both consistent and divergent, our goal is to highlight the need for future research on the mechanisms by which AHR acts as an immunological switch in macrophages. Ultimately, understanding the contexts in which AHR-signaling promotes and/or inhibits differentiation, proinflammatory functions, and immunoregulatory functions, will help uncover functional predictions of immunotoxicity following exposure to environmental chemicals as well as better design AHR-targeted immunotherapies.

Indexed as

Cell DifferentiationMacrophagesReceptors, Aryl HydrocarbonSignal TransductionAnimalsBasic Helix-Loop-Helix ProteinsEnvironmental PollutantsHumansImmunity, InnateAHR protein, humanBasic Helix-Loop-Helix ProteinsEnvironmental PollutantsReceptors, Aryl Hydrocarbonaryl hydrocarbon receptorimmunomodulationimmunosuppressioninflammationmacrophages

Identifiers

PMID38603630
PMCPMC11199922
OpenAlexW4394711380

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.