Evidence map›Paper›PMID 38943728›Full record

ArticleEBioMedicine2024

GABA-mediated inhibition of human CD4

Zhe Jin, Hayma Hammoud, Amol Keshavasa Bhandage, Sergiy Vasylyovych Korol, Olivia Trujeque-Ramos, Stasini Koreli, Zhitao Gong, Azasul Islam Chowdhury, Friederike Andrea Sandbaumhüter, Erik Tomas Jansson and 7 more

Abstract read
In one paragraph

Article in EBioMedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. GABAFrontiers in immunology · 2026
    Article
  6. Article
  7. Inhibition of the NaFrontiers in immunology · 2025
    Article
  8. Review
  9. The role of GABA in type 1 diabetes.Frontiers in endocrinology · 2024
    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

17 authors.

Zhe JinDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Hayma HammoudDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Amol Keshavasa BhandageDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Sergiy Vasylyovych KorolDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Olivia Trujeque-RamosDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Stasini KoreliDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Zhitao GongDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Azasul Islam ChowdhuryDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Friederike Andrea SandbaumhüterDepartment of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden.
Erik Tomas JanssonDepartment of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden.
Robin Sean LindsayDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Gustaf ChristofferssonDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Per Erik AndrénDepartment of Pharmaceutical Biosciences, Spatial Mass Spectrometry, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Per-Ola CarlssonDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Peter BergstenDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Masood Kamali-MoghaddamDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Bryndis BirnirDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden. Electronic address: bryndis.birnir@mcb.uu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundγ-aminobutyric acid (GABA), known as the main inhibitory neurotransmitter in the brain, exerts immunomodulatory functions by interaction with immune cells, including T cells. Metabolic programs of T cells are closely linked to their effector functions including proliferation, differentiation, and cytokine production. The physiological molecules glucose and insulin may provide environmental cues and guidance, but whether they coordinate to regulate GABA-mediated T cell immunomodulation is still being examined.

methodsCD4

findingsWe demonstrate that GABA-mediated reduction of metabolic activity and the release of inflammatory proteins, including IFNγ and IL-10, were abolished in human CD4

interpretationThese findings support that metabolic factors, such as glucose and insulin, influence the GABA-mediated immunomodulation of human primary T cells effector functions.

fundingThe Swedish Children's Diabetes Foundation, The Swedish Diabetes Foundation, The Swedish Research Council 2018-02952, EXODIAB, The Ernfors Foundation, The Thurings Foundation and the Science for Life Laboratory.

Indexed as

CD4-Positive T-LymphocytesDiabetes Mellitus, Type 1gamma-Aminobutyric AcidGlucoseInsulinAdultCytokinesFemaleHumansLymphocyte ActivationMaleReceptors, GABA-ACytokinesgamma-Aminobutyric AcidGlucoseInsulinReceptors, GABA-ACalcium signalingCytokineDiabetesGABA(A) receptorsGlycolysisImmunometabolism

Identifiers

PMID38943728
PMCPMC11260598

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Registered trials

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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.