Evidence map›Paper›PMID 24973821›Full record

ArticleNature immunology2014

The metabolic checkpoint kinase mTOR is essential for IL-15 signaling during the development and activation of NK cells.

Antoine Marçais, Julien Cherfils-Vicini, Charlotte Viant, Sophie Degouve, Sébastien Viel, Aurore Fenis, Jessica Rabilloud, Katia Mayol, Armelle Tavares, Jacques Bienvenu and 4 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 375 papers.

0numbers the graph read from it
0cells of the map it votes in
375citing papers in PubMed
15.2field-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

375 citing papers in PubMed, 589 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Antoine MarçaisCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Julien Cherfils-Vicini *Institute for Research on Cancer and Aging, Nice (IRCAN), Nice University, CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice 06107, France.
Charlotte Viant *Centre d'Immunologie de Marseille-Luminy, INSERM U1104; CNRS UMR7280; Aix Marseille Université, UM2, Marseille, France.
Sophie DegouveCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Sébastien VielCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Aurore FenisCentre d'Immunologie de Marseille-Luminy, INSERM U1104; CNRS UMR7280; Aix Marseille Université, UM2, Marseille, France.
Jessica RabilloudCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Katia MayolCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Armelle TavaresCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Jacques BienvenuLaboratoire d'Immunologie, Hospices Civils de Lyon, Centre Hospitalier Lyon Sud, France.
Yann-Gaël GangloffEcole Normale Supérieure de Lyon, Lyon, France.
Eric GilsonInstitute for Research on Cancer and Aging, Nice (IRCAN), Nice University, CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice 06107, France.
Eric VivierCentre d'Immunologie de Marseille-Luminy, INSERM U1104; CNRS UMR7280; Aix Marseille Université, UM2, Marseille, France.
Thierry WalzerCIRI, Centre International de Recherche en Infectiologie - International Center for Infectiology Research, Lyon, France.
Université Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRÉcole Normale Supérieure de Lyon · FRHospices Civils de Lyon · FR

Funding

European Research Council 281025
6 · The paper itself

Abstract

Interleukin 15 (IL-15) controls both the homeostasis and the peripheral activation of natural killer (NK) cells. The molecular basis for this duality of action remains unknown. Here we found that the metabolic checkpoint kinase mTOR was activated and boosted bioenergetic metabolism after exposure of NK cells to high concentrations of IL-15, whereas low doses of IL-15 triggered only phosphorylation of the transcription factor STAT5. mTOR stimulated the growth and nutrient uptake of NK cells and positively fed back on the receptor for IL-15. This process was essential for sustaining NK cell proliferation during development and the acquisition of cytolytic potential during inflammation or viral infection. The mTORC1 inhibitor rapamycin inhibited NK cell cytotoxicity both in mice and humans; this probably contributes to the immunosuppressive activity of this drug in different clinical settings.

Indexed as

AnimalsCell ProliferationCells, CulturedHerpesviridae InfectionsHumansImmunosuppressive AgentsInflammationInfluenza A Virus, H1N1 SubtypeInterleukin-15Killer Cells, NaturalLymphocyte ActivationMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MiceMice, Inbred C57BLMice, KnockoutImmunosuppressive AgentsInterleukin-15Mechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2mTOR protein, mouseMultiprotein ComplexesPoly I-CSirolimusSTAT5 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID24973821
PMCPMC4110708
OpenAlexW2104825199

What OpenQuestion holds

Textmetadata
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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.