Evidence map›Paper›PMID 26451009›Full record

ReviewInternational immunology2016

Group 3 innate lymphoid cells: regulating host-commensal bacteria interactions in inflammation and cancer.

Jeremy Goc, Matthew R Hepworth, Gregory F Sonnenberg

Open access · bronzeAbstract readReview
In one paragraph

Review in International immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.1field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  14. mTOR Mediates IL-23 Induction of Neutrophil IL-17 and IL-22 Production.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  15. Intestinal bacterium-derived cyp27a1 prevents colon cancer cell apoptosis.American journal of translational research · 2016
    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

3 authors at 1 institution in 1 country.

Jeremy GocJoan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA.
Matthew R HepworthJoan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA.
Gregory F SonnenbergJoan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA gfsonnenberg@med.cornell.edu.
Cornell University · US

Funding

INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR024134 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$70.4M
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
Immune regulation of intestinal health and diseaseR56AI114724 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SONNENBERG, GREGORY F · 2015 to 2015
$424k
NCRR NIH HHS UL1-RR024134NIAID NIH HHS R56 AI114724NIAID NIH HHS R56AI114724NIH HHS DP5 OD012116NIH HHS DP5OD012116Wellcome Trust 105644
6 · The paper itself

Abstract

A delicate balance exists between the mammalian immune system and normally beneficial commensal bacteria that colonize the gastrointestinal tract, which is necessary to maintain tissue homeostasis. Dysregulation of these interactions between the host and commensal bacteria is causally associated with chronic inflammation and the development of cancer. In contrast, recent reports have highlighted that commensal bacteria also play an essential role in promoting anti-tumor immune responses in several contexts, highlighting a paradox whereby interactions between the host and commensal bacteria can influence both pro- and anti-tumor immunity. Given the critical roles for group 3 innate lymphoid cells (ILC3s) in regulating inflammation, tissue repair and host-microbe interactions in the intestine, here we discuss new evidence that ILC3s may profoundly influence the development, progression and control of tumors. In this review, we provide an overview of recent advances in understanding the impact of commensal bacteria on tumorigenesis, discuss recent findings identifying ILC3s as critical regulators of host-microbe interactions and highlight the emerging role of this immune cell population in cancer and their potential implication as a therapeutic target.

Indexed as

ImmunotherapyAnimalsCarcinogenesisHomeostasisHost-Pathogen InteractionsHumansImmunity, InnateInflammationIntestinal MucosaLymphocytesNeoplasmsSymbiosiscancercommensal bacteriainnate lymphoid cellsintestinal homeostasis

Identifiers

PMID26451009
PMCPMC5891988
OpenAlexW2269070698

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.