Evidence map›Paper›PMID 21358638›Full record

ArticleNature immunology2011

The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2.

Greg M Delgoffe, Kristen N Pollizzi, Adam T Waickman, Emily Heikamp, David J Meyers, Maureen R Horton, Bo Xiao, Paul F Worley, Jonathan D Powell

Open access · bronzeAbstract read
In one paragraph

Article in Nature immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 700 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
700citing papers in PubMed, 1 pooled it
29.8field-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

700 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,081 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  16. CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  17. Article
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  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Greg M DelgoffeSidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Kristen N Pollizzi
Adam T Waickman
Emily Heikamp
David J Meyers
Maureen R Horton
Bo Xiao
Paul F Worley
Jonathan D Powell
Johns Hopkins University · USCancer Research Center · USSidney Kimmel Comprehensive Cancer Center · US

Funding

CELLULAR &MOLECULAR MECH OF INFLAMMATORY REACTIONST32AI007247 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Joel L Pomerantz · 1985 to 2026
$10.2M
A central role for mTOR in Determining T Cell Activation versus ToleranceR01AI077610 · NIAID · JOHNS HOPKINS UNIVERSITY · PI POWELL, JONATHAN D · 2009 to 2019
$4.0M
NIAID NIH HHS R01 AI077610NIAID NIH HHS R01AI077610-01A2NIAID NIH HHS T32 AI007247
6 · The paper itself

Abstract

The kinase mTOR has emerged as an important regulator of the differentiation of helper T cells. Here we demonstrate that differentiation into the T(H)1 and T(H)17 subsets of helper T cells was selectively regulated by signaling from mTOR complex 1 (mTORC1) that was dependent on the small GTPase Rheb. Rheb-deficient T cells failed to generate T(H)1 and T(H)17 responses in vitro and in vivo and did not induce classical experimental autoimmune encephalomyelitis (EAE). However, they retained their ability to become T(H)2 cells. Alternatively, when mTORC2 signaling was deleted from T cells, they failed to generate T(H)2 cells in vitro and in vivo but preserved their ability to become T(H)1 and T(H)17 cells. Our data identify mechanisms by which two distinct signaling pathways downstream of mTOR regulate helper cell fate in different ways. These findings define a previously unknown paradigm that links T cell differentiation with selective metabolic signaling pathways.

Indexed as

Cell DifferentiationSignal TransductionAnimalsCarrier ProteinsCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleFlow CytometryImmunoblottingMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutMonomeric GTP-Binding ProteinsMultiprotein ComplexesCarrier ProteinsCrtc2 protein, mouseCytokinesMechanistic Target of Rapamycin Complex 1Monomeric GTP-Binding ProteinsmTOR protein, mouseMultiprotein ComplexesNeuropeptidesProteinsRapamycin-Insensitive Companion of mTOR ProteinRas Homolog Enriched in Brain ProteinRheb protein, mouserictor protein, mouseTOR Serine-Threonine KinasesTrans-ActivatorsTranscription Factors

Identifiers

PMID21358638
PMCPMC3077821
OpenAlexW2155759076

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.