Evidence map›Paper›PMID 26595889›Full record

ArticleNature immunology2016

Complementarity and redundancy of IL-22-producing innate lymphoid cells.

Lucille C Rankin, Mathilde J H Girard-Madoux, Cyril Seillet, Lisa A Mielke, Yann Kerdiles, Aurore Fenis, Elisabeth Wieduwild, Tracy Putoczki, Stanislas Mondot, Olivier Lantz and 14 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
12.6field-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.

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

162 citing papers in PubMed, 241 citations in OpenAlex.

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  16. GPX4 restricts ferroptosis of NKp46Cell death & disease · 2024
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102 more citing papers are in PubMed but not listed here.

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

24 authors at 8 institutions in 5 countries.

Lucille C RankinThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Mathilde J H Girard-MadouxCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
Cyril SeilletThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Lisa A MielkeThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Yann KerdilesCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
Aurore FenisCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
Elisabeth WieduwildCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
Tracy PutoczkiThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Stanislas MondotLabex Milieu Intérieur, Institut Pasteur, Paris, France.
Olivier LantzLaboratoire d'Immunologie and Inserm U932, Institut Curie, Paris, France.
Dieter DemonInflammation Research Center, VIB, Ghent University, Ghent, Belgium.
Anthony T PapenfussThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.ORCID http://orcid.org/0000-0002-1102-8506
Gordon K SmythThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.ORCID http://orcid.org/0000-0001-9221-2892
Mohamed LamkanfiInflammation Research Center, VIB, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-4898-7663
Sebastian CarottaThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Jean-Christophe RenauldLudwig Institute for Cancer Research and Experimental Medicine Unit, Catholic University of Louvain, Brussels, Belgium.ORCID http://orcid.org/0000-0003-1736-2131
Wei ShiThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Sabrina CarpentierMI-mAbs consortium Aix-Marseille University, Centre d'Immunologie de Marseille-Luminy, Marseille, France.
Tim SoosBioinnovation, SANOFI, Boston, Massachusetts, USA.
Christopher ArendtBioinnovation, SANOFI, Boston, Massachusetts, USA.
Sophie UgoliniCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
Nicholas D HuntingtonThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Gabrielle T BelzThe Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Eric VivierCentre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
The University of Melbourne · AUCentre National de la Recherche Scientifique · FREduInnovation · USGhent University · BEAix-Marseille Université · FRInserm · FRInstitut Pasteur · FRLudwig Cancer Research · BE

Funding

European Research Council 268537
6 · The paper itself

Abstract

Intestinal T cells and group 3 innate lymphoid cells (ILC3 cells) control the composition of the microbiota and gut immune responses. Within the gut, ILC3 subsets coexist that either express or lack the natural cytoxicity receptor (NCR) NKp46. We identified here the transcriptional signature associated with the transcription factor T-bet-dependent differentiation of NCR(-) ILC3 cells into NCR(+) ILC3 cells. Contrary to the prevailing view, we found by conditional deletion of the key ILC3 genes Stat3, Il22, Tbx21 and Mcl1 that NCR(+) ILC3 cells were redundant for the control of mouse colonic infection with Citrobacter rodentium in the presence of T cells. However, NCR(+) ILC3 cells were essential for cecal homeostasis. Our data show that interplay between intestinal ILC3 cells and adaptive lymphocytes results in robust complementary failsafe mechanisms that ensure gut homeostasis.

Indexed as

Immunity, InnateAnimalsCitrobacter rodentiumCluster AnalysisDisease Models, AnimalEnterobacteriaceae InfectionsFemaleGene Expression ProfilingGene Expression RegulationHomeostasisInterleukin-22InterleukinsLymphocytesLymphocyte SubsetsMaleMiceInterleukin-22InterleukinsMyeloid Cell Leukemia Sequence 1 ProteinNatural Cytotoxicity Triggering Receptor 1T-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID26595889
PMCPMC4720992
OpenAlexW2268221626

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.