Evidence map›Paper›PMID 29672155›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2018

An endogenous aryl hydrocarbon receptor ligand, ITE, induces regulatory T cells and ameliorates experimental colitis.

Jessica D Abron, Narendra P Singh, Manoj K Mishra, Robert L Price, Mitzi Nagarkatti, Prakash S Nagarkatti, Udai P Singh

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

47 citing papers in PubMed, 68 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Jessica D AbronPathology, Microbiology and Immunology, School of Medicine, University of South Carolina , Columbia, South Carolina.
Narendra P SinghPathology, Microbiology and Immunology, School of Medicine, University of South Carolina , Columbia, South Carolina.
Manoj K MishraDepartment of Biological Sciences, Alabama State University , Montgomery, Alabama.
Robert L PriceCell Biology and Anatomy, School of Medicine, University of South Carolina , Columbia, South Carolina.
Mitzi NagarkattiPathology, Microbiology and Immunology, School of Medicine, University of South Carolina , Columbia, South Carolina.
Prakash S NagarkattiPathology, Microbiology and Immunology, School of Medicine, University of South Carolina , Columbia, South Carolina.
Udai P SinghPathology, Microbiology and Immunology, School of Medicine, University of South Carolina , Columbia, South Carolina.
University of South Carolina · USAlabama State University · US

Funding

Targeting early ceramide elevation in pre-symptomatic eczemaP20GM103641 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ENOS, REILLY, NAGARKATTI, PRAKASH S · 2012 to 2023
$20.7M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
AhR ligands in epigenetic dysregulation of T cellsR01AI123947 · NIAID · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI, NAGARKATTI, PRAKASH S · 2017 to 2021
$1.8M
Immune Mechanism Underlying CXCR3 and its Ligand Mediated Interstitial CystitisR56DK087836 · NIDDK · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI SINGH, UDAI P. · 2012 to 2012
$123k
NCCIH NIH HHS P01 AT003961NIAID NIH HHS R01 AI123947NIDDK NIH HHS R56 DK087836NIGMS NIH HHS P20 GM103641
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition that affects millions of people with high morbidity and health care costs. The precise etiology of IBD is unknown, but clear evidence suggests that intestinal inflammation is caused by an excessive immune response to mucosal antigens. Recent studies have shown that activation of the aryl hydrocarbon receptor (AhR) induces regulatory T cells (Tregs) and suppresses autoimmune diseases. In the current study, we investigated if a nontoxic ligand of AhR, 2-(1' H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE), can attenuate dextran sodium sulfate-induced colitis. Our studies demonstrated that in mice that received ITE treatment in vivo, colitis pathogenesis, including a decrease in body weight, was significantly reversed along with the systemic and intestinal inflammatory cytokines. ITE increased the expression of Tregs in spleen, mesenteric lymph nodes (MLNs), and colon lamina propria lymphocytes (cLPL) of mice with colitis when compared with controls. This induction of Tregs was reversed by AhR antagonist treatment in vitro. ITE treatment also increased dendritic cells (CD11c

Indexed as

ColitisIndolesThiazolesAnimalsAnti-Inflammatory AgentsAutoimmunityInflammatory Bowel DiseasesInterleukinsIntestinal MucosaLigandsMiceReceptors, Aryl HydrocarbonT-Lymphocytes, Regulatory2-(1'H-indole-3'-carbonyl)thiazole-4-carboxylic acid methyl esterAnti-Inflammatory AgentsIndolesInterleukinsLigandsReceptors, Aryl HydrocarbonThiazolesCrohn’s diseaseinflammatory bowel diseaseTh1/Th17ulcerative colitis

Identifiers

PMID29672155
PMCPMC6139639
OpenAlexW2801129478

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.