Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [ATAC-seq]

ABSTRACT: HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [ATAC-seq]

PROVIDER: PRJNA996658 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25344608_1.fastq.gz	Fastqsanger.gz
	SRR25344608_2.fastq.gz	Fastqsanger.gz
	SRR25344609_1.fastq.gz	Fastqsanger.gz
	SRR25344609_2.fastq.gz	Fastqsanger.gz
	SRR25344610_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer.

Project description:HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer.

| PRJNA996657 | ENA

HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [RNA-seq]

Project description:HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [RNA-seq]

| PRJNA996659 | ENA

HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [RNA-seq]

Project description:Transcriptional and epigenetic features were detected in WT versus HMGB2-/- P14 T cells following LCMV Arm and Cl13 infection.

2023-07-24 | GSE237812 | GEO

HMGB2 regulates the differentiation and stemness of exhausted CD8+ T cells during chronic viral infection and cancer [ATAC-seq]

Project description:Transcriptional and epigenetic features were detected in WT versus HMGB2-/- P14 T cells following LCMV Arm and Cl13 infection.

2023-07-24 | GSE237811 | 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

A core stemness program in exhausted CD8+ T cells

Project description:A core stemness program in exhausted CD8+ T cells

| PRJNA1201764 | ENA

HMGB2 regulates the differentiation and stemness of exhausted CD8<sup>+</sup> T cells during chronic viral infection and cancer.

Project description:Chronic infections and cancers evade the host immune system through mechanisms that induce T cell exhaustion. The heterogeneity within the exhausted CD8+ T cell pool has revealed the importance of stem-like progenitor (Tpex) and terminal (Tex) exhausted T cells, although the mechanisms underlying their development are not fully known. Here we report High Mobility Group Box 2 (HMGB2) protein expression is upregulated and sustained in exhausted CD8+ T cells, and HMGB2 expression is critical for their differentiation. Through epigenetic and transcriptional programming, we identify HMGB2 as a cell-intrinsic regulator of the differentiation and maintenance of Tpex cells during chronic viral infection and in tumors. Despite Hmgb2-/- CD8+ T cells expressing TCF-1 and TOX, these master regulators were unable to sustain Tpex differentiation and long-term survival during persistent antigen. Furthermore, HMGB2 also had a cell-intrinsic function in the differentiation and function of memory CD8+ T cells after acute viral infection. Our findings show that HMGB2 is a key regulator of CD8+ T cells and may be an important molecular target for future T cell-based immunotherapies.

| S-EPMC10499904 | biostudies-literature

Chronic viral infection of naive, effector, memory and exhausted virus-specific CD8 T cells

Project description:CD8 T cells normally differentiate from resting naïve 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. Keywords: infection response

2007-11-27 | GSE9650 | GEO

ATAC-Seq profiling of progenitor exhausted and terminally exhausted CD8+ T-cells from tumors and chronic viral infection

Project description:Epigenetically similar subpopulations of exhausted CD8+ T-cells are found in chronic viral infection and tumors

2018-12-02 | GSE123236 | GEO

Redox sensor KEAP1 promotes stemness and prevents reductive stress in exhausted CD8+ T cells via inhibiting NRF2

Project description:Persistent antigen stimulation exposes CD8+ T cells to various metabolic stresses and induces a dysfunctional state termed T-cell exhaustion. Exhausted CD8+ T cells are continuously replenished by a recently discovered self-renewing stem-like CD8+ T-cell subset, which maintains long-term immunity and provides proliferative burst in response to immunotherapies. Although the redox system plays an important role in regulating T-cell activation, how cellular redox affects the differentiation of stem-like and exhausted CD8+ T cells is incompletely understood. Here, we showed that both antigen stimulation and terminal differentiation reduced mitochondrial oxidation and reactive oxygen species (ROS) in exhausted CD8+ T cells, which displayed a chromatin state primed for regulation by the redox sensing KEAP1-NRF2 pathway. During chronic viral infection, KEAP1 promoted expansion of antiviral CD8+ T cells and facilitated their differentiation into the stem-like subset in a cell autonomous manner. In addition, KEAP1 was required for establishing proper transcriptional programs of stem-like and exhausted CD8+ T cells. Mechanistically, KEAP1 maintained oxidation by upregulating genes involved in mitochondrial oxidation and repressing NRF2-driven transcription of antioxidant pathways. Deleting KEAP1 binding domain in NRF2 released NRF2 from regulation by KEAP1, impaired expansion and stemness of CD8+ T cells, and dysregulated multiple metabolic pathways including redox pathways. Thus, our study revealed a novel role of the redox pathway in regulating the molecular program and differentiation of stem-like and exhausted CD8+ T cells during chronic antigen stimulation.

2024-11-11 | GSE224756 | GEO

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