Evidence map›Paper›PMID 27601261›Full record

ArticleNature communications2016

NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation.

Meixiang Yang, Shasha Chen, Juan Du, Junming He, Yuande Wang, Zehua Li, Guangao Liu, Wanwen Peng, Xiaokang Zeng, Dan Li and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
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  10. Article
  11. Review
  12. Checkpoint TIPE2 Limits the Helper Functions of NK Cells in Supporting Antitumor CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  13. Article
  14. Review
  15. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

16 authors at 4 institutions in 1 country.

Meixiang YangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Shasha ChenInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Juan DuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Junming HeBiomedical Translational Research Institute, Jinan University, Guangzhou 510632, China.
Yuande WangBiomedical Translational Research Institute, Jinan University, Guangzhou 510632, China.
Zehua LiInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Guangao LiuBiomedical Translational Research Institute, Jinan University, Guangzhou 510632, China.
Wanwen PengBiomedical Translational Research Institute, Jinan University, Guangzhou 510632, China.
Xiaokang ZengBiomedical Translational Research Institute, Jinan University, Guangzhou 510632, China.
Dan LiInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Panglian XuSchool of Medicine, Tsinghua University, Beijing 100086, China.
Wei GuoSchool of Medicine, Tsinghua University, Beijing 100086, China.
Zai ChangCenter of Animal Facility, Tsinghua University, Beijing 100086, China.
Song WangCollaborative Innovation Center, Wuhan Sports University, Wuhan 340036, China.
Zhigang TianSchool of Life Sciences, University of Sciences and Technology of China, Hefei 230026, China.
Zhongjun DongInstitute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
Tsinghua University · CNJinan University · CNUniversity of Science and Technology of China · CNWuhan Sports University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of metabolic signalling by IL-15 is required for natural killer (NK) cell development. Here we show that Tsc1, a repressor of mTOR, is dispensable for the terminal maturation, survival and function of NK cells but is critical to restrict exhaustive proliferation of immature NK cells and activation downstream of IL-15 during NK cell development. Tsc1 is expressed in immature NK cells and is upregulated by IL-15. Haematopoietic-specific deletion of Tsc1 causes a marked decrease in the number of NK cells and compromises rejection of 'missing-self' haematopoietic tumours and allogeneic bone marrow. The residual Tsc1-null NK cells display activated, pro-apoptotic phenotype and elevated mTORC1 activity. Deletion of Raptor, a component of mTORC1, largely reverses these defects. Tsc1-deficient NK cells express increased levels of T-bet and downregulate Eomes and CD122, a subunit of IL-15 receptor. These results reveal a role for Tsc1-dependent inhibition of mTORC1 activation during immature NK cell development.

Indexed as

AnimalsApoptosisB-LymphocytesGene Expression RegulationHematopoiesisInterleukin-15Interleukin-2 Receptor beta SubunitKiller Cells, NaturalMechanistic Target of Rapamycin Complex 1Melanoma, ExperimentalMiceMice, KnockoutProtein SubunitsT-Box Domain ProteinsT-LymphocytesTuberous Sclerosis Complex 1 ProteinEomes protein, mouseIl2rb protein, mouseInterleukin-15Interleukin-2 Receptor beta SubunitMechanistic Target of Rapamycin Complex 1Protein SubunitsT-Box Domain ProteinsTsc1 protein, mouseTuberous Sclerosis Complex 1 ProteinTumor Suppressor Proteins

Identifiers

PMID27601261
PMCPMC5023956
OpenAlexW2515467040

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.