PXD041654 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | GABA, glucose and insulin orchestrate CD4+ T cells effector functions |
Description | Metabolic programs of immune cells are closely linked to their effector functions , where physiological molecules provide environmental cues and guidance. Exactly how it happens is still being unraveled. Insulin maintains normal blood glucose levels and glucose is themain source of energy and a precursor for many biomolecules in T cells, whereas γ-aminobutyric acid (GABA), best known as a neurotransmitter, is increasingly recognized as a regulatory molecule in the immune system. Here, we demonstrate that GABA-mediated reduction of metabolic activity and release of inflammatory molecules, including IFNγ and IL-10, was abolished in human CD4+ T cells, when the glucose concentration was elevated above normal levels. In a glucose concentration-dependent manner, insulin enhanced the GABAA receptors activated currents and GABA-dependent Ca2+ influx. GABA decreased, whereas insulin maintained glycolysis but in a SGLT (Na + -glucose transporter)-dependent manner, revealing expression of SGLTs in activated CD4+ T cells. The SGLTs antagonist phlorizin, alone or together with GABA, restored the inhibition of IFNγ and IL-10 release in presence of high glucose. This study exposes concerted effects of GABA, glucose and insulin on CD4+ T cells metabolic activity and release of inflammatory molecules, and identifies a role for SGLTs in CD4+ T cells function. |
HostingRepository | PRIDE |
AnnounceDate | 2024-08-10 |
AnnouncementXML | Submission_2024-08-10_12:49:46.880.xml |
DigitalObjectIdentifier | https://dx.doi.org/10.6019/PXD041654 |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Supported dataset by repository |
PrimarySubmitter | Erik Jansson |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | amidated residue; acetylated residue; monohydroxylated residue; deamidated residue; iodoacetamide derivatized residue |
Instrument | MALDI Synapt MS |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2023-04-19 09:50:18 | ID requested | |
⏵ 1 | 2024-08-10 12:49:47 | announced | |
2 | 2024-10-22 06:54:23 | announced | 2024-10-22: Updated project metadata. |
Publication List
10.1016/j.ebiom.2024.105217; |
Jin Z, Hammoud H, Bhandage AK, Korol SV, Trujeque-Ramos O, Koreli S, Gong Z, Chowdhury AI, Sandbaumh, ü, ter FA, Jansson ET, Lindsay RS, Christoffersson G, Andr, é, n PE, Carlsson PO, Bergsten P, Kamali-Moghaddam M, Birnir B, T cell functions is enhanced by insulin but impaired by high glucose levels. EBioMedicine, 105():105217(2024) [pubmed] |
10.6019/PXD041654; |
Keyword List
submitter keyword: CD4, GABA |
Contact List
Erik Jansson |
contact affiliation | Department of Pharmaceutical Biosciences, Uppsala University |
contact email | erik.jansson@farmbio.uu.se |
lab head | |
Erik Jansson |
contact affiliation | Uppsala University |
contact email | erik.jansson@farmbio.uu.se |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
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PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD041654
- Label: PRIDE project
- Name: GABA, glucose and insulin orchestrate CD4+ T cells effector functions