Evidence map›Paper›PMID 27783115›Full record

ArticleArchives of toxicology2017

Aryl hydrocarbon receptor signaling modifies Toll-like receptor-regulated responses in human dendritic cells.

Sarah Kado, W L William Chang, Aimy Nguyen Chi, Monika Wolny, David M Shepherd, Christoph F A Vogel

Erratum issuedAbstract read
In one paragraph

Article in Archives of toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  8. Mechanisms and Recent Advances of Small-Molecule Therapeutics in Rosacea Treatment.Clinical, cosmetic and investigational dermatology · 2025
    Review
  9. Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Tolerogenic dendritic cells generatedFrontiers in immunology · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The aryl hydrocarbon receptor facilitates the human cytomegalovirus-mediated G1/S block to cell cycle progression.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Sarah KadoCenter for Health and the Environment, University of California Davis, One Shields Avenue, Davis, CA 95616, USA.
W L William ChangCenter for Comparative Medicine, University of California, One Shields Avenue, Davis, CA 95616, USA.
Aimy Nguyen ChiCenter for Health and the Environment, University of California Davis, One Shields Avenue, Davis, CA 95616, USA.
Monika WolnyCenter for Health and the Environment, University of California Davis, One Shields Avenue, Davis, CA 95616, USA.
David M ShepherdDepartment of Biomedical and Pharmaceutical Sciences, University of Montana, Missoula, MT, 59812, USA.
Christoph F A VogelCenter for Health and the Environment, University of Montana, Missoula, MT, 59812, USA. cfvogel@ucdavis.edu.
University of California, Davis · USUniversity of Montana · US

Funding

Development of a novel platform for the delivery of AhR antagonists to DCs and T cellsR01ES013784 · NIEHS · UNIVERSITY OF MONTANA · PI SHEPHERD, DAVID M · 2006 to 2017
$4.0M
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 ES013784NIEHS NIH HHS R01 ES019898
6 · The paper itself

Abstract

Currently, it is not well understood how ligands of the aryl hydrocarbon receptor (AhR) modify inflammatory responses triggered by Toll-like receptor (TLR) agonists in human dendritic cells (DCs). Here, we show that AhR ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the tryptophan derivatives 6-formylindolo[3,2-b] carbazole (FICZ), kynurenine (kyn), and the natural dietary compound indole-3-carbinol (I3C) differentially modify cytokine expression in human monocyte-derived DCs (MoDCs). The results show that TLR-activated MoDCs express higher levels of AhR and are more sensitive toward the effects of AhR ligands. Depending on the cytokine, treatment with AhR ligands led to a synergistic or antagonistic effect of the TLR-triggered response in MoDCs. Thus, activation of AhR increased the expression of interleukin (IL)-1β, but decreased the expression of IL-12A in TLR-activated MoDCs. Furthermore, TCDD and FICZ may have opposite effects on the expression of cytochrome P4501A1 (CYP1A1) in TLR8-activated MoDCs indicating that the effect of the specific AhR ligand may depend on the presence of the specific TLR agonist. Gene silencing showed that synergistic effects of AhR ligands on TLR-induced expression of IL-1β require a functional AhR and the expression of NF-κB RelB. On the other hand, repression of IL-12A by TCDD and FICZ involved the induction of the caudal type homeobox 2 (CDX2) transcription factor. Additionally, the levels of DC surface markers were decreased in MoDCs by TCDD, FICZ and I3C, but not by kyn. Overall, these data demonstrate that AhR modulates TLR-induced expression of cytokines and DC-specific surface markers in MoDCs involving NFκB RelB and the immune regulatory factor CDX2.

Indexed as

CarbazolesCDX2 Transcription FactorCells, CulturedCytokinesDendritic CellsDose-Response Relationship, DrugGene Expression RegulationHumansInterleukin-1betaKynurenineLipopolysaccharidesPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonSignal TransductionToll-Like Receptor 3Toll-Like Receptors6-formylindolo(3,2-b)carbazoleCarbazolesCDX2 protein, humanCDX2 Transcription FactorCytokinesInterleukin-1betaKynurenineLipopolysaccharidesPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRELB protein, humanTLR3 protein, humanToll-Like Receptor 3Toll-Like ReceptorsTranscription Factor RelBAhRCDX2CytokinesDendritic cellsNF-κBTLR

Identifiers

PMID27783115
PMCPMC5400689
OpenAlexW4243627407

What OpenQuestion holds

Textmetadata
LicenceTDM
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.