Evidence map›Paper›PMID 24962260›Full record

ReviewNature reviews. Immunology2014

Integrating canonical and metabolic signalling programmes in the regulation of T cell responses.

Kristen N Pollizzi, Jonathan D Powell

Abstract readReview
In one paragraph

Review in Nature reviews. Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers.

0numbers the graph read from it
0cells of the map it votes in
248citing papers in PubMed
31.5field-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

248 citing papers in PubMed, 367 citations in OpenAlex.

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  9. Do Metastatic Cells Arise from PD-L1International journal of molecular sciences · 2026
    Review
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  20. Understanding and Managing Hyper IgE Syndromes.ImmunoTargets and therapy · 2025
    Review

188 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

2 authors at 1 institution in 1 country.

Kristen N PollizziSidney Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Jonathan D PowellSidney Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Johns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
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
Transplantation tolerance and immune function following mTOR inhibition.R01AI091481 · NIAID · JOHNS HOPKINS UNIVERSITY · PI POWELL, JONATHAN D · 2010 to 2013
$1.6M
NCI NIH HHS P30 CA006973NIAID NIH HHS R01 AI077610NIAID NIH HHS R01AI077610‑01A2NIAID NIH HHS R01 AI091481NIAID NIH HHS T32 AI007247
6 · The paper itself

Abstract

Over the past decade, our understanding of T cell activation, differentiation and function has markedly expanded, providing a greater appreciation of the signals and pathways that regulate these processes. It has become clear that evolutionarily conserved pathways that regulate stress responses, metabolism, autophagy and survival have crucial and specific roles in regulating T cell responses. Recent studies suggest that the metabolic pathways involving MYC, hypoxia-inducible factor 1α (HIF1α), AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are activated upon antigen recognition and that they are required for directing the consequences of T cell receptor engagement. The purpose of this Review is to provide an integrated view of the role of these metabolic pathways and of canonical T cell signalling pathways in regulating the outcome of T cell responses.

Indexed as

AMP-Activated Protein KinasesAnimalsCD8-Positive T-LymphocytesCell DifferentiationGlycolysisHypoxia-Inducible Factor 1, alpha SubunitImmunologic MemoryLymphocyte ActivationMiceProto-Oncogene Proteins c-mycReceptors, Antigen, T-CellSignal TransductionT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesAMP-Activated Protein KinasesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, mouseMyc protein, mouseProto-Oncogene Proteins c-mycReceptors, Antigen, T-CellTOR Serine-Threonine Kinases

Identifiers

PMID24962260
PMCPMC4390057
OpenAlexW2046959528

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.