Evidence map›Paper›PMID 36766792›Full record

ArticleCells2023

T Cell Energy Metabolism Is a Target of Glucocorticoids in Mice, Healthy Humans, and MS Patients.

Leonie Meyer-Heemsoth, Katja Mitschke, Jasmina Bier, Konstantin Schütz, Andreas Villunger, Tobias J Legler, Martin S Weber, Fred Lühder, Holger M Reichardt

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. 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

9 authors at 3 institutions in 2 countries.

Leonie Meyer-HeemsothInstitute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany.
Katja MitschkeInstitute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany.
Jasmina BierInstitute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany.ORCID 0000-0003-2330-0797
Konstantin SchützDepartment of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany.
Andreas VillungerInstitute of Developmental Immunology, Medical University of Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0001-8259-4153
Tobias J LeglerDepartment of Transfusion Medicine, University Medical Center Göttingen, 37075 Göttingen, Germany.ORCID 0000-0002-1408-5397
Martin S WeberDepartment of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany.
Fred LühderInstitute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany.ORCID 0000-0001-6103-9425
Holger M ReichardtInstitute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany.ORCID 0000-0003-4647-057X
Universitätsmedizin Göttingen · DEFraunhofer Institute for Translational Medicine and Pharmacology · DEInnsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids (GCs) are used to treat inflammatory disorders such as multiple sclerosis (MS) by exerting prominent activities in T cells including apoptosis induction and suppression of cytokine production. However, little is known about their impact on energy metabolism, although it is widely accepted that this process is a critical rheostat of T cell activity. We thus tested the hypothesis that GCs control genes and processes involved in nutrient transport and glycolysis. Our experiments revealed that escalating doses of dexamethasone (Dex) repressed energy metabolism in murine and human primary T cells. This effect was mediated by the GC receptor and unrelated to both apoptosis induction and Stat1 activity. In contrast, treatment of human T cells with rapamycin abolished the repression of metabolic gene expression by Dex, unveiling mTOR as a critical target of GC action. A similar phenomenon was observed in MS patients after intravenous methylprednisolon (IVMP) pulse therapy. The expression of metabolic genes was reduced in the peripheral blood T cells of most patients 24 h after GC treatment, an effect that correlated with disease activity. Collectively, our results establish the regulation of T cell energy metabolism by GCs as a new immunomodulatory principle.

Indexed as

GlucocorticoidsMultiple SclerosisAnimalsDexamethasoneEnergy MetabolismHumansMiceT-LymphocytesDexamethasoneGlucocorticoidsglucocorticoidsmetabolismmultiple sclerosisT cells

Identifiers

PMID36766792
PMCPMC9914408
OpenAlexW4318485549

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.