Evidence map›Paper›PMID 20498003›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2010

Aryl hydrocarbon receptor activation reduces dendritic cell function during influenza virus infection.

Guang-Bi Jin, Amanda J Moore, Jennifer L Head, Joshua J Neumiller, B Paige Lawrence

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  3. Review
  4. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. AHR Regulates NK Cell MigrationFrontiers in immunology · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 2 institutions in 1 country.

Guang-Bi JinDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.
Amanda J Moore
Jennifer L Head
Joshua J Neumiller
B Paige Lawrence
University of Rochester · USWashington State University · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Infectious Diseases and Microbial Immunology Training ProgramT32AI007025 · NIAID · WASHINGTON STATE UNIVERSITY · PI Thomas H KAWULA, M KARIUKI NJENGA · 1985 to 2026
$7.4M
Environmental Influences on Epigenetic Immune ProgrammingR01ES017250 · NIEHS · UNIVERSITY OF ROCHESTER · PI LAWRENCE, B PAIGE · 2011 to 2015
$1.8M
Ah receptor-mediated deregulation of lactogenesisR01ES013958 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B PAIGE · 2005 to 2009
$1.7M
MECHANISMS OF TCDD PULMONARY IMMUNOTOXICITYR01ES010619 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B. PAIGE · 2000 to 2004
$1.2M
Mechanisms by which TCDD impairs immunological memoryK02ES012409 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B PAIGE · 2005 to 2009
$619k
NIAID NIH HHS T32-AI07025NIEHS NIH HHS K02 ES012409NIEHS NIH HHS K02-ES012409NIEHS NIH HHS P30 ES001247NIEHS NIH HHS P30-ES01247NIEHS NIH HHS R01-ES013958NIEHS NIH HHS R01 ES017250NIEHS NIH HHS R01-ES10619
6 · The paper itself

Abstract

It has long been known that activation of the aryl hydrocarbon receptor (AhR) by ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppresses T cell-dependent immune responses; however, the underlying cellular targets and mechanism remain unclear. We have previously shown that AhR activation by TCDD reduces the proliferation and differentiation of influenza virus-specific CD8(+) T cells through an indirect mechanism; suggesting that accessory cells are critical AhR targets during infection. Respiratory dendritic cells (DCs) capture antigen, migrate to lymph nodes, and play a key role in activating naive CD8(+) T cells during respiratory virus infection. Herein, we report an examination of how AhR activation alters DCs in the lung and affects their trafficking to and function in the mediastinal lymph nodes (MLN) during infection with influenza virus. We show that AhR activation impairs lung DC migration and reduces the ability of DCs isolated from the MLN to activate naive CD8(+) T cells. Using novel AhR mutant mice, in which the AhR protein lacks its DNA-binding domain, we show that the suppressive effects of TCDD require that the activated AhR complex binds to DNA. These new findings suggest that AhR activation by chemicals from our environment impacts DC function to stimulate naive CD8(+) T cells and that immunoregulatory genes within DCs are critical targets of AhR. Moreover, our results reinforce the idea that environmental signals and AhR ligands may contribute to differential susceptibilities and responses to respiratory infection.

Indexed as

AnimalsCD8-Positive T-LymphocytesCell MovementDendritic CellsFemaleLymph NodesLymphocyte ActivationMiceMice, Inbred C57BLOrthomyxoviridae InfectionsPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID20498003
PMCPMC2905408
OpenAlexW2103273228

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.