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Nutrient-driven histone code determines exhausted CD8+ T cell fates [RNA-seq]

ABSTRACT: Nutrient-driven histone code determines exhausted CD8+ T cell fates [RNA-seq]

PROVIDER: PRJNA984165 | ENA |

REPOSITORIES: ENA

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Nutrient-driven histone code determines exhausted CD8+ T cell fates

Project description:Nutrient-driven histone code determines exhausted CD8+ T cell fates

| PRJNA984020 | ENA

Nutrient-driven histone code determines exhausted CD8+ T cell fates [ChIP-seq]

Project description:Nutrient-driven histone code determines exhausted CD8+ T cell fates [ChIP-seq]

| PRJNA984164 | ENA

Nutrient-driven histone code determines exhausted CD8+ T cell fates [RNA-seq]

Project description:To investigate the role of ACSS2NLS in the regulation of CD8+ T cell responses in B16-GP33 tumor model Exhausted T cells (TEX) in cancer and chronic viral infections undergo metabolic and epigenetic remodeling, impairing protective capabilities. However, the impact of nutrient metabolism on epigenetic modifications that control TEX differentiation remains unclear. Our study reveals that TEX cells shift from acetate to citrate metabolism by downregulating acetyl-CoA synthetase 2 (ACSS2) while maintaining ATP-citrate lyase (ACLY) activity. This metabolic switch increases citrate-dependent histone acetylation, mediated by histone acetyltransferase KAT2A-ACLY interactions, at TEX signature-genes while reducing acetate-dependent histone acetylation, dependent on p300-ACSS2 complexes, at effector and memory T cell genes. Nuclear ACSS2 overexpression or ACLY inhibition prevents TEX differentiation and enhances tumor-specific T cell responses. These findings unveil a nutrient-driven histone code governing CD8+ T cell differentiation, with implications for metabolic- and epigenetic-based T cell therapies

2024-12-11 | GSE235006 | GEO

Nutrient-driven histone code determines exhausted CD8+ T cell fates [ChIP-seq]

Project description:To investigate the role of ACSS2 and ACLY in the regulation of epigenetic states of CD8+ T cells in cancer and chronic viral infections Exhausted T cells (TEX) in cancer and chronic viral infections undergo metabolic and epigenetic remodeling, impairing protective capabilities. However, the impact of nutrient metabolism on epigenetic modifications that control TEX differentiation remains unclear. Our study reveals that TEX cells shift from acetate to citrate metabolism by downregulating acetyl-CoA synthetase 2 (ACSS2) while maintaining ATP-citrate lyase (ACLY) activity. This metabolic switch increases citrate-dependent histone acetylation, mediated by histone acetyltransferase KAT2A-ACLY interactions, at TEX signature-genes while reducing acetate-dependent histone acetylation, dependent on p300-ACSS2 complexes, at effector and memory T cell genes. Nuclear ACSS2 overexpression or ACLY inhibition prevents TEX differentiation and enhances tumor-specific T cell responses. These findings unveil a nutrient-driven histone code governing CD8+ T cell differentiation, with implications for metabolic- and epigenetic-based T cell therapies

2024-12-11 | GSE235005 | GEO

Nutrient-driven histone code determines exhausted CD8+ T cell fates

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

2024-12-11 | GSE235007 | GEO

Single-cell RNA-seq of human breast tumor samples with exhausted and non-exhausted immune environments

Project description:Fresh human breast tumor tissue was dissociated into single cells and viably frozen. Patient samples were annotated as having an ""exhausted"" or ""non-exhausted"" immune environment based on CyTOF characterization of T cell phenotypes (Wagner et al, Cell 2019). 14 samples (7 exhausted, 7 non-exhausted) were selected for scRNA-seq (without prior cell type enrichment) with the goal to compare the two immune environment types and to comprehensively characterize exhaustion-associated features of the tumor microenvironment.

2023-08-25 | E-MTAB-10607 | biostudies-arrayexpress

Endothelial Cell Cycle State Determines Propensity for Arterial-Venous Fates (ATAC-Seq)

Project description:Endothelial Cell Cycle State Determines Propensity for Arterial-Venous Fates (ATAC-Seq)

| PRJNA873054 | ENA

Intestinal epithelial c-Maf expression determines enterocyte differentiation and nutrient uptake

Project description:Intestinal epithelial c-Maf expression determines enterocyte differentiation and nutrient uptake

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Learning the sequence code for mRNA and protein abundance in human immune cells

Project description:mRNA and protein abundance are defined by transcriptional and post-transcriptional regulatory mechanisms. Here, we develop a machine learning pipeline, termed SONAR, to decipher the endogenous sequence code that determines mRNA and protein abundance in human cells. SONAR models predict up to 62% of mRNA and 63% of protein abundance independent of promoter or enhancer information, and reveal a strong—yet dynamic—cell-type specific sequence code. We also find that the effect of sequence features is dependent on their location within the mRNA transcript. Using SONAR, we design synthetic 3’UTRs, with which protein expression levels can be manipulated and tailored to a specific cell-type. Beyond its fundamental findings, our work provides novel means to improve immunotherapies and biotechnology applications.

2023-09-20 | GSE240919 | GEO

Transcription profiling of mouse naive, effector, memory and exhausted virus-specific CD8 T cells after chronic viral infection

Project description:CD8 T cells normally differentiate from resting naÃ¯ve T cells into function effector and then memory CD8 T cells following acute infections. During chronic viral infections, however, virus-specific CD8 T cells often become exhausted. We used microarrays to examine the gene expression differences between naive, effector, memory and exhausted virus-specific CD8 T cells following lymphocytic choriomeningitis virus infection. Experiment Overall Design: Three or four independent samples were sorted by flow cytometry for each cell type (naive, effector, memory and exhausted) virus-specific CD8 T cells. RNA was extracted and hybridized to Affymetrix microarrays.

2008-06-16 | E-GEOD-9650 | biostudies-arrayexpress

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