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

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

PROVIDER: PRJNA996657 | ENA |

REPOSITORIES: ENA

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			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

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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 [ATAC-seq]

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

| PRJNA996658 | 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

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