Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation

ABSTRACT: Investigating the effect of reducing ketolytic capacity on the transcriptional profile of CD8 T cells responding to listeria infection in vivo

ORGANISM(S): Mus musculus

PROVIDER: GSE212048 | GEO | 2025/07/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation [ChIP-seq]

Project description:Investigating the effects of Bdh1 deletion on acetylation of lysine 27 on histone 3 (H3K27ac) in CD8+ T cells 24 h post-activation with anti-CD3 and anti-CD28 antibodies

2025-07-09 | GSE229358 | GEO

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation

Project description:Environmental nutrient availability influences T cell metabolism, impacting T cell function and shaping immune outcomes. However, the metabolic pathways critical for optimal T cell responses remain poorly understood. Here, we identify ketone bodies (KBs) – including -hydroxybutyrate (OHB) and acetoacetate (AcAc) – as essential fuels supporting CD8+ T cell metabolism and effector function. Ketolysis is an intrinsic feature of highly functional CD8+ T effector (Teff) cells and OHB directly increases CD8+ Teff cell IFN- production and cytolytic activity. Using metabolic tracers, we establish that CD8+ Teff cells preferentially use KBs over glucose to fuel the tricarboxylic acid (TCA) cycle in vitro and in vivo. KBs directly boost the respiratory capacity of CD8+ T cells and TCA cycle-dependent metabolic pathways that fuel T cell growth. Mechanistically, we find that OHB is a major substrate for acetyl-CoA production in CD8+ T cells and regulates effector responses through effects on histone acetylation. Together, our results identify cell-intrinsic ketolysis as a metabolic and epigenetic driver of optimal CD8+ T cell effector responses.

2023-10-11 | PXD036292 | Pride

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation.

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-07-09 | GSE229359 | GEO

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation.

Project description:Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation.

| PRJNA954061 | ENA

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation

Project description:Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation

| PRJNA873701 | ENA

Ketolysis drives CD8<sup>+</sup> T cell effector function through effects on histone acetylation.

Project description:Environmental nutrient availability influences T cell metabolism, impacting T cell function and shaping immune outcomes. Here, we identified ketone bodies (KBs)-including β-hydroxybutyrate (βOHB) and acetoacetate (AcAc)-as essential fuels supporting CD8+ T cell metabolism and effector function. βOHB directly increased CD8+ T effector (Teff) cell cytokine production and cytolytic activity, and KB oxidation (ketolysis) was required for Teff cell responses to bacterial infection and tumor challenge. CD8+ Teff cells preferentially used KBs over glucose to fuel the tricarboxylic acid (TCA) cycle in vitro and in vivo. KBs directly boosted the respiratory capacity and TCA cycle-dependent metabolic pathways that fuel CD8+ T cell function. Mechanistically, βOHB was a major substrate for acetyl-CoA production in CD8+ T cells and regulated effector responses through effects on histone acetylation. Together, our results identify cell-intrinsic ketolysis as a metabolic and epigenetic driver of optimal CD8+ T cell effector responses.

| S-EPMC10528215 | biostudies-literature

Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation [ChIP-seq]

Project description:Ketolysis is a metabolic driver of CD8+ T cell effector function through histone acetylation [ChIP-seq]

| PRJNA954063 | ENA

Memory CD8+ T cells upregulate glycolysis and effector functions under limiting oxygen conditions

Project description:Memory CD8+ T cells are indispensable for maintaining long-term immunity against intracellular pathogens and tumors. Despite their presence in oxygen-deprived tissues of infection sites or tumors, the impact of local oxygen pressure on memory CD8+ T cells has remained largely unclear. We sought to elucidate how oxygen pressure impacted memory CD8+ T cells arising after infection with Listeria monocytogenes-OVA. Our data revealed that reduced oxygen pressure during in vitro culture switched CD8+ T cell metabolism from an OXPHOS to a glycolytic phenotype. Quantitative proteomic analysis showed that limiting oxygen conditions increased the expression of glucose transporters and components of the glycolytic pathway, while decreasing TCA cycle and mitochondrial respiratory chain proteins. The altered CD8+ T cell metabolism did not affect the expansion potential, but enhanced the granzyme B and IFN- production capacity. Memory CD8+ T cells cultured under low oxygen pressure were able to persist long-term in vivo and provided protection against bacterial rechallenge. Taken together, our study indicates that strategies of cellular immune therapy may benefit from reducing oxygen during culture to develop memory CD8+ T cells with superior effector functions .

2022-12-01 | PXD032236 | Pride

Expression profiling of WT and Dot1L KO CD8 effector T cells and H3K79me2 occupancy in WT effector CD8 T cells

Project description:We studied the role of the histone methyltransferase DOT1L in T cell development and differentiation. We generated RNA-seq data from sorted CD8 effector T cells from WT (Lck-cre+/-) and Dot1L KO (Lck-cre+/-;Dot1Lfl/fl) mice infected with Listeria monocytogenes. This data was compared with H3K79me2 ChIP-seq data from the same T cell subset.

2021-08-01 | GSE155406 | GEO

Notch regulates cytolytic effector function in CD8+ T cells.

Project description:The maturation of naive CD8(+) T cells into effector CTLs is a critical feature of a functional adaptive immune system. Development of CTLs depends, in part, upon the expression of the transcriptional regulator eomesodermin (EOMES), which is thought to regulate expression of two key effector molecules, perforin and granzyme B. Although EOMES is important for effector CTL development, the precise mechanisms regulating CD8(+) effector cell maturation remains poorly understood. In this study, we show that Notch1 regulates the expression of EOMES, perforin, and granzyme B through direct binding to the promoters of these crucial effector molecules. By abrogating Notch signaling, both biochemically as well as genetically, we conclude that Notch activity mediates CTL activity through direct regulation of EOMES, perforin, and granzyme B.

| S-EPMC4374745 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data