Evidence map›Paper›PMID 32709928›Full record

ArticleCommunications biology2020

T cell-specific deletion of Pgam1 reveals a critical role for glycolysis in T cell responses.

Koji Toriyama, Makoto Kuwahara, Hiroshi Kondoh, Takumi Mikawa, Nobuaki Takemori, Amane Konishi, Toshihiro Yorozuya, Takeshi Yamada, Tomoyoshi Soga, Atsushi Shiraishi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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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

11 authors at 5 institutions in 1 country.

Koji ToriyamaDepartment of Ophthalmology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, 791-0295, Japan.
Makoto KuwaharaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan.
Hiroshi KondohGeriatric Unit, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Takumi MikawaGeriatric Unit, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Nobuaki TakemoriAdvanced Research Center, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan.
Amane KonishiDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan.
Toshihiro YorozuyaDepartment of Anesthesia and Perioperative Medicine, Graduate School of Medicine, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan.
Takeshi YamadaDepartment of Infection and Host Defenses, Graduate School of Medicine, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan.
Tomoyoshi SogaInstitute for Advanced Bioscience, Keio University, Tsuruoka City, Yamagata, 997-0052, Japan.
Atsushi ShiraishiDepartment of Ophthalmology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, 791-0295, Japan.
Masakatsu YamashitaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon City, Ehime, 791-0295, Japan. yamamasa@m.ehime-u.ac.jp.ORCID http://orcid.org/0000-0002-8975-3513
Ehime University · JPKyoto University · JPEhime Prefectural University of Health Science · JPEhime University Hospital · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the important roles of glycolysis in T cells have been demonstrated, the regulatory mechanism of glycolysis in activated T cells has not been fully elucidated. Furthermore, the influences of glycolytic failure on the T cell-dependent immune response in vivo remain unclear. We therefore assessed the role of glycolysis in the T cell-dependent immune response using T cell-specific Pgam1-deficient mice. Both CD8 and CD4 T cell-dependent immune responses were attenuated by Pgam1 deficiency. The helper T cell-dependent inflammation was ameliorated in Pgam1-deficient mice. Glycolysis augments the activation of mTOR complex 1 (mTORC1) and the T-cell receptor (TCR) signals. Glutamine acts as a metabolic hub in activated T cells, since the TCR-dependent increase in intracellular glutamine is required to augment glycolysis, increase mTORC1 activity and augment TCR signals. These findings suggest that mTORC1, glycolysis and glutamine affect each other and cooperate to induce T cell proliferation and differentiation.

Indexed as

AnimalsCell DifferentiationCell ProliferationGlycolysisHumansImmunityLymphocyte ActivationMechanistic Target of Rapamycin Complex 1MicePhosphoglycerate MutaseT-LymphocytesMechanistic Target of Rapamycin Complex 1Phosphoglycerate Mutasephosphoglycerate mutase 1, human

Identifiers

PMID32709928
PMCPMC7382475
OpenAlexW3044564615

What OpenQuestion holds

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LicenceCC BY
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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.