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Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

ABSTRACT: Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

PROVIDER: PRJNA490747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7827000.fastq.gz	Fastqsanger.gz
	SRR7827001.fastq.gz	Fastqsanger.gz
	SRR7826992.fastq.gz	Fastqsanger.gz
	SRR7827002.fastq.gz	Fastqsanger.gz
	SRR7826993.fastq.gz	Fastqsanger.gz

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Similar Datasets

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

| PRJNA490745 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

| PRJNA490749 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [single-cell RNA-seq]

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [single-cell RNA-seq]

| PRJNA490748 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

Project description:Stem-like CD8 T cells maintain long-term antiviral CD8 immunity during chronic infection, and share regulatory pathways with memory precursor effector cells generated after acute infection. However, it is unclear whether stem-like CD8 T cells require distinct transcriptional and epigenetic regulation for their longevity and adaptation to the immunosuppressive environment in chronic infection. Here, our comparison of single-cell transcriptomes and epigenetic profiles of CD8 T cells responding to acute and chronic viral infections revealed that stem-like CD8 T cells became distinct from memory precursors before clonal expansion ended. We found that a coexpression gene module containing Tox exhibited higher transcriptional activities and active histone marks in stem-like T cells than memory precursors. Moreover, TOX promoted persistence of antiviral CD8 T cells, and was required for stem-like CD8 differentiation. Our results indicate that stem-like CD8 T cells require unique transcriptional and epigenetic programs for their differentiation and persistence during chronic viral infection.

2019-04-16 | GSE119942 | GEO

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

2019-04-16 | GSE119941 | GEO

Innate lymphoid cell development requires TOX-dependent generation of a common ILC progenitor

Project description:Subtypes of innate lymphoid cells (ILC), defined by effector function and transcription factor expression, have recently been identified. In the adult, ILC derive from common lymphoid progenitors in bone marrow, although transcriptional regulation of the developmental pathways involved remains poorly defined. TOX is required for development of lymphoid tissue inducer cells, a type of ILC3 required for lymph node organogenesis, and NK cells, a type of ILC1. We show here that production of multiple ILC lineages requires TOX, as a result of TOX-dependent development of common ILC progenitors. Comparative transcriptome analysis demonstrated failure to induce various aspects of the ILC gene program in the absence of TOX, implicating this nuclear factor as a key early determinant of ILC lineage specification. TOX KO vs. wild tyype

2015-04-27 | E-GEOD-65850 | biostudies-arrayexpress

Oncogenic role of TOX in CTCL

Project description:TOX is a nuclear factor essential for the development of CD4+ T cells in the thymus. TOX is found to be aberrantly up-regulated in the skin biopsies and in the blood CD4+ T cells of cutaneous T cell lymphoma. The goal of this study is to identify potential transcriptional targets of TOX in CTCL by comparison between TOX shRNA transfected CTCL cells (Hut78 and HH) and control CTCL cells. Two color experiment. Lentivirus transduced control vector vs. TOX shRNA vectors on Hut78 and HH cell lines. Biological replicates: 3 control replicates, 3 shRNA tansduced replicates for each cell line.

2014-04-29 | E-GEOD-57122 | biostudies-arrayexpress

Innate lymphoid cell development requires TOX-dependent generation of a common ILC progenitor

2015-04-27 | GSE65850 | GEO

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

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

2019-04-16 | GSE119943 | GEO

TNFR2 loss prevents TOX upregulation in CD8+TIM3+ T cells and affords improved responses to tumor and chronic LCMV

Project description:Preview PDF Abstract Exhaustion represents a collection of programmed T cell differentiation states and an important mode of T cell dysfunction. T cell progression from progenitor to terminal exhaustion is associated with upregulation of the transcription factor TOX and expression of TIM3. Our understanding of factors regulating TOX expression and the transition from progenitor to terminal exhaustion, however, remains incomplete. We reveal here that T cell upregulation of tumor necrosis factor receptor type II (TNFR2) coincides with the gain of phenotypic markers and functions reflective of terminal exhaustion. Meanwhile, knocking out TNFR2 affords a novel population of T cells that express TIM3 but possess diminished TOX levels and functional characteristics of both progenitor and terminally exhausted cells. TIM3+ TNFR2 KO T cells exhibit reduced exhaustion transcriptional programs and enhanced AP1 pathway signatures. Finally, TNFR2 KO mice demonstrate improved T cell-dependent control of tumor and chronic lymphocytic choriomeningitis viral (cLCMV) infection, while pharmacologic antagonism of TNFR2 licenses responses to checkpoint blockade in multiple tumor models.

2025-05-19 | GSE297330 | GEO

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