Evidence map›Paper›PMID 25908663›Full record

ArticleScience (New York, N.Y.)2015

Immune tolerance. Group 3 innate lymphoid cells mediate intestinal selection of commensal bacteria-specific CD4⁺ T cells.

Matthew R Hepworth, Thomas C Fung, Samuel H Masur, Judith R Kelsen, Fiona M McConnell, Juan Dubrot, David R Withers, Stephanie Hugues, Michael A Farrar, Walter Reith and 5 more

Abstract read
In one paragraph

Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed, 1 pooled it
22.1field-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.

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

333 citing papers in PubMed, 1 synthesis or guideline pooled it, 500 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Matthew R HepworthJill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Gastroenterology Division, and Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY, USA.
Thomas C FungJill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Gastroenterology Division, and Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY, USA. Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Samuel H MasurDivision of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Judith R KelsenDivision of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Fiona M McConnellMedical Research Council, Centre for Immune Regulation, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Juan DubrotDepartment of Pathology and Immunology, University of Geneva Medical School, Geneva, Switzerland.
David R WithersMedical Research Council, Centre for Immune Regulation, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Stephanie HuguesDepartment of Pathology and Immunology, University of Geneva Medical School, Geneva, Switzerland.
Michael A FarrarCenter for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, MN, USA.
Walter ReithDepartment of Pathology and Immunology, University of Geneva Medical School, Geneva, Switzerland.
Gérard EberlInstitut Pasteur, Microenvironment and Immunity Unit, Paris, France.
Robert N BaldassanoDivision of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Terri M LauferPerelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Philadelphia Veterans Affairs Medical Center, Philadelphia, PA, USA.
Charles O ElsonDepartments of Medicine and Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Gregory F SonnenbergJill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Gastroenterology Division, and Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY, USA. gfsonnenberg@med.cornell.edu.
Children's Hospital of Philadelphia · USUniversity of Geneva · CHInstitut Pasteur · FRUniversity of Pennsylvania · USVeterans Health Administration · US

Funding

INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR024134 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$70.4M
INNATE AND ADAPTIVE MICROBIAL IMMUNITY IN IBDP01DK071176 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ELSON, CHARLES O · 2005 to 2014
$12.5M
Regulation of host-commensal relationships in human health and diseaseDP5OD012116 · OD · WEILL MEDICAL COLL OF CORNELL UNIV · PI SONNENBERG, GREGORY F · 2012 to 2016
$2.1M
NCRR NIH HHS UL1 RR024134NCRR NIH HHS UL1-RR024134NIDDK NIH HHS DK071176NIDDK NIH HHS P01 DK071176NIH HHS DP5 OD012116NIH HHS DP5OD012116Wellcome Trust
6 · The paper itself

Abstract

Inflammatory CD4(+) T cell responses to self or commensal bacteria underlie the pathogenesis of autoimmunity and inflammatory bowel disease (IBD), respectively. Although selection of self-specific T cells in the thymus limits responses to mammalian tissue antigens, the mechanisms that control selection of commensal bacteria-specific T cells remain poorly understood. Here, we demonstrate that group 3 innate lymphoid cell (ILC3)-intrinsic expression of major histocompatibility complex class II (MHCII) is regulated similarly to thymic epithelial cells and that MHCII(+) ILC3s directly induce cell death of activated commensal bacteria-specific T cells. Further, MHCII on colonic ILC3s was reduced in pediatric IBD patients. Collectively, these results define a selection pathway for commensal bacteria-specific CD4(+) T cells in the intestine and suggest that this process is dysregulated in human IBD.

Indexed as

Immunity, InnateAnimalsApoptosisAutoimmunityBacteriaCD4-Positive T-LymphocytesColonFemaleFlagellinHistocompatibility Antigens Class IIHumansInflammatory Bowel DiseasesLymphocyte ActivationMaleMiceMice, Inbred C57BLCBir1 flagellinFlagellinHistocompatibility Antigens Class II

Identifiers

PMID25908663
PMCPMC4449822
OpenAlexW2075691631

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.