Evidence map›Paper›PMID 33303820›Full record

ArticleScientific reports2020

Long-term T cell fitness and proliferation is driven by AMPK-dependent regulation of reactive oxygen species.

Anouk Lepez, Tiphène Pirnay, Sébastien Denanglaire, David Perez-Morga, Marjorie Vermeersch, Oberdan Leo, Fabienne Andris

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. The influence of metabolic disorders on adaptive immunity.Cellular & molecular immunology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. STAT3 modulates CD4Aging cell · 2023
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. The Natural History of T Cell Metabolism.International journal of molecular sciences · 2021
    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

7 authors at 1 institution in 1 country.

Anouk LepezULB Centre for Research in Immunology (U-CRI), Université Libre de Bruxelles, Brussels, Belgium.
Tiphène PirnayULB Centre for Research in Immunology (U-CRI), Université Libre de Bruxelles, Brussels, Belgium.
Sébastien DenanglaireULB Centre for Research in Immunology (U-CRI), Université Libre de Bruxelles, Brussels, Belgium.
David Perez-MorgaCentre for Microscopy and Molecular Imaging (CMMI), Université Libre de Bruxelles, Brussels, Belgium.
Marjorie VermeerschCentre for Microscopy and Molecular Imaging (CMMI), Université Libre de Bruxelles, Brussels, Belgium.
Oberdan LeoULB Centre for Research in Immunology (U-CRI), Université Libre de Bruxelles, Brussels, Belgium.
Fabienne AndrisULB Centre for Research in Immunology (U-CRI), Université Libre de Bruxelles, Brussels, Belgium. Fabienne.Andirs@ulb.be.
Université Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AMP-activated kinase (AMPK) is a major energy sensor metabolic enzyme that is activated early during T cell immune responses but its role in the generation of effector T cells is still controversial. Using both in vitro and in vivo models of T cell proliferation, we show herein that AMPK is dispensable for early TCR signaling and short-term proliferation but required for sustained long-term T cell proliferation and effector/memory T cell survival. In particular, AMPK promoted accumulation of effector/memory T cells in competitive homeostatic proliferation settings. Transplantation of AMPK-deficient hematopoïetic cells into allogeneic host recipients led to a reduced graft-versus-host disease, further bolstering a role for AMPK in the expansion and pathogenicity of effector T cells. Mechanistically, AMPK expression enhances the mitochondrial membrane potential of T cells, limits reactive oxygen species (ROS) production, and resolves ROS-mediated toxicity. Moreover, dampening ROS production alleviates the proliferative defect of AMPK-deficient T cells, therefore indicating a role for an AMPK-mediated ROS control of T cell fitness.

Indexed as

AMP-Activated Protein KinasesCell ProliferationCells, CulturedCell SurvivalGene ExpressionHumansMembrane Potential, MitochondrialReactive Oxygen SpeciesReceptors, Antigen, T-CellSignal TransductionT-LymphocytesAMP-Activated Protein KinasesReactive Oxygen SpeciesReceptors, Antigen, T-Cell

Identifiers

PMID33303820
PMCPMC7728748
OpenAlexW3112799247

What OpenQuestion holds

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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.