Evidence map›Paper›PMID 22177117›Full record

ArticleImmunity2012

The aryl hydrocarbon receptor regulates gut immunity through modulation of innate lymphoid cells.

Ju Qiu, Jennifer J Heller, Xiaohuan Guo, Zong-ming E Chen, Kamonwan Fish, Yang-Xin Fu, Liang Zhou

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03059862 (The Role of Tryptophan on Aryl Hydrocarbon Receptor Activation), which is not on this map. Cited by 546 papers.

0numbers the graph read from it
0cells of the map it votes in
546citing papers in PubMed
16.6field-weighted citation impact, top 1% 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.

NCT03059862 nacompletednot on this mapstarted 2017, after this paper: background citation

The Role of Tryptophan on Aryl Hydrocarbon Receptor Activation: a Randomized, Double Blind, Placebo-controlled, Crossover Design Pilot Trial

TypeinterventionalSponsorMcMaster UniversityRan2017 to 2018Enrolled20ConditionsDiet ModificationArmsL-tryptophan, Placebo
3 · Its place in the literature

Who cites it

546 citing papers in PubMed, 824 citations in OpenAlex.

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486 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ju QiuDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Jennifer J Heller
Xiaohuan Guo
Zong-ming E Chen
Kamonwan Fish
Yang-Xin Fu
Liang Zhou
Northwestern University · USUniversity of Chicago · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
CELLULAR &MOLECULAR BASIS OF DISEASE TRAINING PROGRAMT32GM008061 · NIGMS · NORTHWESTERN UNIVERSITY · PI CARTHEW, RICHARD W. · 1985 to 2022
$17.1M
AhR activation in Th17 and Treg cell differentiationR01AI089954 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ZHOU, LIANG · 2010 to 2014
$1.9M
ROLE OF AHR IN T LYMPHOCYTE DEVELOPMENT AND FUNCTIONR01DK105562 · NIDDK · UNIVERSITY OF FLORIDA · PI ZHOU, LIANG · 2015 to 2019
$1.8M
TNF family members for lymph angiogenesis and lymph node hypertrophyR01CA141975 · NCI · UNIVERSITY OF CHICAGO · PI FU, YANG-XIN · 2010 to 2014
$1.6M
The Role of Negative Signal in Early InfectionR21AI090392 · NIAID · UNIVERSITY OF CHICAGO · PI FU, YANG-XIN · 2010 to 2011
$427k
The Role of the Aryl Hydrocarbon Receptor in Intestinal ImmunityR21AI091962 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ZHOU, LIANG · 2011 to 2012
$419k
NCI NIH HHS CA141975NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA141975NIAID NIH HHS AI 089954NIAID NIH HHS AI090392NIAID NIH HHS AI091962NIAID NIH HHS R01 AI089954NIAID NIH HHS R21 AI090392NIAID NIH HHS R21 AI091962NIDDK NIH HHS R01 DK105562NIGMS NIH HHS T32 GM008061
6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) expressing the nuclear receptor RORγt are essential for gut immunity presumably through production of interleukin-22 (IL-22). The molecular mechanism underlying the development of RORγt(+) ILCs is poorly understood. Here, we have shown that the aryl hydrocarbon receptor (Ahr) plays an essential role in RORγt(+) ILC maintenance and function. Expression of Ahr in the hematopoietic compartment was important for accumulation of adult but not fetal intestinal RORγt(+) ILCs. Without Ahr, RORγt(+) ILCs had increased apoptosis and less production of IL-22. RORγt interacted with Ahr and promoted Ahr binding at the Il22 locus. Upon IL-23 stimulation, Ahr-deficient RORγt(+) ILCs had reduced IL-22 expression, consistent with downregulation of IL-23R in those cells. Ahr-deficient mice succumbed to Citrobacter rodentium infection, whereas ectopic expression of IL-22 protected animals from early mortality. Our data uncover a previously unrecognized physiological role for Ahr in promoting innate gut immunity by regulating RORγt(+) ILCs.

Indexed as

Immunity, InnateAnimalsCitrobacter rodentiumEnterobacteriaceae InfectionsGastrointestinal TractGene DeletionInterleukin-22InterleukinsLymphocytesMiceMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl HydrocarbonInterleukin-22InterleukinsNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl Hydrocarbon

Identifiers

PMID22177117
PMCPMC3268875
OpenAlexW1981177186

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.