Evidence map›Paper›PMID 24302727›Full record

ArticleThe Journal of biological chemistry2014

Cross-talk between aryl hydrocarbon receptor and the inflammatory response: a role for nuclear factor-κB.

Christoph F A Vogel, Elaine M Khan, Patrick S C Leung, M Eric Gershwin, W L William Chang, Dalei Wu, Thomas Haarmann-Stemmann, Alexander Hoffmann, Michael S Denison

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

164 citing papers in PubMed, 1 synthesis or guideline pooled it, 262 citations in OpenAlex.

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  9. Glycyrrhizic Acid Alleviates Atherosclerosis inInternational journal of molecular sciences · 2026
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104 more citing papers are in PubMed but not listed here.

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 6 institutions in 2 countries.

Christoph F A VogelFrom the Department of Environmental Toxicology.
Elaine M Khan
Patrick S C Leung
M Eric Gershwin
W L William Chang
Dalei Wu
Thomas Haarmann-Stemmann
Alexander Hoffmann
Michael S Denison
Center for Rheumatology · USLeibniz Institute of Environmental Medicine · DEUniversity of California, Davis · USSanford Burnham Prebys Medical Discovery Institute · USSociety of Environmental Toxicology and Chemistry · USUniversity of California, Los Angeles · US

Funding

RECOMBINANT DETECTION SYSTEMS FOR DIOXIN LIKE CHEMICALSR01ES007685 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI DENISON, MICHAEL STEVEN · 1995 to 2019
$4.7M
Importance of AhR for the cellular function and communication of dendritic cellsR01ES019898 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2012 to 2016
$1.7M
NIEHS NIH HHS R01 ES007685NIEHS NIH HHS R01 ES019898NIEHS NIH HHS R01 ES019898-02
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is involved in the regulation of immune responses, T-cell differentiation, and immunity. Here, we show that inflammatory stimuli such as LPS induce the expression of AhR in human dendritic cells (DC) associated with an AhR-dependent increase of CYP1A1 (cytochrome P4501A1). In vivo data confirmed the elevated expression of AhR by LPS and the LPS-enhanced 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated induction of CYP1A1 in thymus of B6 mice. Inhibition of nuclear factor-κB (NF-κB) repressed both normal and LPS-enhanced, TCDD-inducible, AhR-dependent gene expression and canonical pathway control of RelA-regulated AhR-responsive gene expression. LPS-mediated induction of AhR was NF-κB-dependent, as shown in mouse embryonic fibroblasts (MEFs) derived from Rel null mice. AhR expression and TCDD-mediated induction of CYP1A1 was significantly reduced in RelA-deficient MEF compared with wild type MEF cells and ectopic expression of RelA restored the expression of AhR and induction of CYP1A1 in MEF RelA null cells. Promoter analysis of the human AhR gene identified three putative NF-κB-binding elements upstream of the transcription start site. Mutation analysis of the AhR promoter identified one NF-κB site as responsible for mediating the induction of AhR expression by LPS and electrophoretic shift assays demonstrated that this NF-κB motif is recognized by the RelA/p50 heterodimer. Our results show for the first time that NF-κB RelA is a critical component regulating the expression of AhR and the induction of AhR-dependent gene expression in immune cells illustrating the interaction of AhR and NF-κB signaling.

Indexed as

Signal TransductionAnimalsBasic Helix-Loop-Helix ProteinsCell LineCytochrome P-450 CYP1A1Dendritic CellsGene Expression RegulationHumansInflammationLipopolysaccharidesMiceMice, KnockoutMutationPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonResponse Elements1,2,7,8-tetrachlorodibenzo-p-dioxinAHR protein, humanAhr protein, mouseBasic Helix-Loop-Helix ProteinsCYP1A1 protein, humanCytochrome P-450 CYP1A1LipopolysaccharidesPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRELA protein, humanRela protein, mouseTranscription Factor RelAAryl Hydrocarbon ReceptorDendritic CellsGene RegulationInflammationNF-Kappa B (NF-KB)

Identifiers

PMID24302727
PMCPMC3894361
OpenAlexW2073563548

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.