Evidence map›Paper›PMID 25492937›Full record

Trial reportJournal of leukocyte biology2015

Foxp3-mediated inhibition of Akt inhibits Glut1 (glucose transporter 1) expression in human T regulatory cells.

Samik Basu, Britany Hubbard, Ethan M Shevach

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 62 citations in OpenAlex.

  1. [Pirfenidone inhibits bladder cancer xenograft growth in mice by regulating regulatory T cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  2. Review
  3. Review
  4. Nutrients: Signal 4 in T cell immunity.The Journal of experimental medicine · 2024
    Article
  5. Review
  6. The Role of PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma Metabolism.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. CD4Precision clinical medicine · 2022
    Review
  11. Review
  12. Review
  13. Review
  14. Metformin to decrease COVID-19 severity and mortality: Molecular mechanisms and therapeutic potential.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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

3 authors at 2 institutions in 1 country.

Samik BasuLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Britany HubbardLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Ethan M ShevachLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA eshevach@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Studies of Human T Regulatory CellsZIAAI001046 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHEVACH, ETHAN · 2009 to 2025
$10.5M
Intramural NIH HHS
6 · The paper itself

Abstract

CD4(+)CD25(+)Foxp3(+) Tregs have a diminished capacity to activate the PI3K/Akt pathway. Although blunted Akt activity is necessary to maintain Treg function, the consequences of this altered signaling are unclear. Glut1 is a cell-surface receptor responsible for facilitating glucose transport across plasma membranes, whose expression is tightly coupled to costimulatory signals and Akt phosphorylation. Freshly isolated human Tregs were unable to up-regulate Glut1 in response to TCR and costimulatory signals compared with Tconv. Consequently, the ability of Tregs to use glucose was also reduced. Introduction of Foxp3 into Tconv inhibited Akt activation and Glut1 expression, indicating that Foxp3 can regulate Glut1. Finally, pharmacologic activation of Akt in Tregs can induce Glut1, overcoming the effects of Foxp3. Together, these results illustrate the molecular basis behind differential glucose metabolism in Tregs.

Indexed as

Cell MembraneEnzyme ActivationFemaleForkhead Transcription FactorsGlucose Transporter Type 1HumansMaleProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellT-Lymphocytes, RegulatoryUp-RegulationForkhead Transcription FactorsFOXP3 protein, humanGlucose Transporter Type 1Proto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSLC2A1 protein, humanautoimmunitylymphocytemetabolismsignal transduction

Identifiers

PMID25492937
PMCPMC4304425
OpenAlexW2316651388

What OpenQuestion holds

Textmetadata
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.