Evidence map›Paper›PMID 21948866›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2011

Dietary ligands of the aryl hydrocarbon receptor induce anti-inflammatory and immunoregulatory effects on murine dendritic cells.

Jenna M Benson, David M Shepherd

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Phytochemicals FromFrontiers in nutrition · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Landscape of AhR Regulators and Coregulators to Fine-Tune AhR Functions.International journal of molecular sciences · 2021
    Review
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Jenna M BensonDepartment of Biomedical and Pharmaceutical Sciences, Center for Environmental Health Sciences, University of Montana, Missoula, Montana 59812, USA.
David M Shepherd
University of Montana · US

Funding

THE ROLE OF PULMONARY SUBPOPULATIONS AND TH2 IMMUNITY IN BALB/C SILICOSIS MODELP20RR017670 · NCRR · UNIVERSITY OF MONTANA · PI HOLIAN, ANDRIJ · 2002 to 2011
$22.0M
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
Consequences of aryl hydrocarbon receptor activation in Crohn's diseaseF31AT005557 · NCCIH · UNIVERSITY OF MONTANA · PI BENSON, JENNA MARIE · 2010 to 2011
$45k
NCCIH NIH HHS F31AT005557NCRR NIH HHS P20 RR017670NIEHS NIH HHS ES013784
6 · The paper itself

Abstract

Activation of the aryl hydrocarbon receptor (AhR) in immune cells, such as dendritic cells (DCs), can lead to suppressed immune responses. Although AhR activation is most recognized for mediating the effects of its prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), many compounds existing in dietary sources can also bind the AhR. Because the immunomodulatory effects of indole-3-carbinol (I3C) and indirubin-3'-oxime (IO) have yet to be investigated in DCs, we evaluated the potential immunomodulatory effects of these compounds on murine DCs. We hypothesized that I3C and IO suppress immune and inflammatory responses in DCs. We found that both I3C and IO decreased the expression of CD11c, CD40, and CD54 while they increased expression of MHC2 and CD80. Following lipopolysaccharide (LPS)-activation, I3C and IO suppressed the production of pro-inflammatory mediators including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-12, and nitric oxide but increased IL-10 levels. These effects of I3C and IO were partially mediated by the AhR. Additionally, immunoregulatory genes, such as ALDH1A, IDO and TGFB, were upregulated following treatment with I3C or IO. Both I3C and IO decreased basal levels of nuclear factor-kappa B p65, but only I3C suppressed the LPS-induced activity of RelB. Finally, when cultured with naïve T cells, bone marrow-derived dendritic cells treated with the dietary AhR ligands increased the frequency of Foxp3+ Tregs in an antigen-specific manner. Taken together, these results indicate that I3C and IO exhibit immunosuppressive and anti-inflammatory effects on DCs. Because I3C and IO are significantly less toxic than TCDD, these natural products may ultimately become useful therapeutics for the treatment of autoimmune and inflammatory diseases.

Indexed as

DietAnimalsAnti-Inflammatory Agents, Non-SteroidalCells, CulturedCoculture TechniquesCytokinesDendritic CellsFlow CytometryImmunosuppressive AgentsIndolesLigandsMiceMice, Inbred C57BLMice, KnockoutNF-kappa BOximesAnti-Inflammatory Agents, Non-SteroidalCytokinesImmunosuppressive Agentsindirubin-3'-monoximeindole-3-carbinolIndolesLigandsNF-kappa BOximesReceptors, Aryl Hydrocarbon

Identifiers

PMID21948866
PMCPMC3216417
OpenAlexW2129820724

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.