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Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [WT vs KO +/- Tim3]

ABSTRACT: Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [WT vs KO +/- Tim3]

PROVIDER: PRJNA545703 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9165560.fastq.gz	Fastqsanger.gz
	SRR9165570.fastq.gz	Fastqsanger.gz
	SRR9165561.fastq.gz	Fastqsanger.gz
	SRR9165571.fastq.gz	Fastqsanger.gz
	SRR9165562.fastq.gz	Fastqsanger.gz

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Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [WT vs KO +/- Tim3]

Project description:Chronic CD8 T-cell stimulation in persisting infections or tumors can induce a stable gene expression program, known as T-cell dysfunction or exhaustion, that limits the cell’s effector functions and anti-viral and anti-tumor immunity. Thus far, the underlaying molecular mechanisms that induce and stabilize this phenotype are vaguely understood. We report here that establishing this program requires the thymocyte selection-associated high mobility group-box protein (Tox). Genetic disruption of Tox augments effector function, decreases the expression of PD-1, and significantly enhances immunopathology. These changes are linked to a failure in fixing the dysfunctional phenotype in the critical Tcf1+ progenitor population and to impaired epigenetic programing. Surprisingly, the gains in effector function co-incide with declining numbers of Tcf1+ cells and result ultimately in reduced total numbers of pathogen-specific T-cells. Thus, we establish Tox as a critical factor for the development of T-cell dysfunction and establish a clear link between CD8 T-cell intrinsic suppression of effector function and protection against immune-pathology.

2019-07-03 | GSE132033 | GEO

Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [ToxKO vs WT Day 20]

Project description:Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [ToxKO vs WT Day 20]

| PRJNA545702 | ENA

Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [KO vs WT Day 8]

Project description:Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [KO vs WT Day 8]

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Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [ToxKO vs WT Day 20]

2019-07-03 | GSE132032 | GEO

Tox reinforces the phenotype and longevity of dysfunctional T cell populations during chronic viral infection [KO vs WT Day 8]

2019-07-03 | GSE132030 | GEO

Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection

Project description:Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection

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Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [ATAC-seq]

Project description:Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [ATAC-seq]

| PRJNA544256 | ENA

Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [Bisulfite-Seq]

Project description:Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [Bisulfite-Seq]

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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

Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [ATAC-seq]

2019-07-03 | GSE131638 | GEO