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Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [ATACseq]

ABSTRACT: Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [ATACseq]

PROVIDER: PRJNA1093468 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28504800_1.fastq.gz	Fastqsanger.gz
	SRR28504800_2.fastq.gz	Fastqsanger.gz
	SRR28504801_1.fastq.gz	Fastqsanger.gz
	SRR28504801_2.fastq.gz	Fastqsanger.gz
	SRR28504802_1.fastq.gz	Fastqsanger.gz

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Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [ATACseq]

Project description:Durability of an antitumor immune response is mediated in part by the persistence of progenitor exhausted CD8 T cells (Tpex). Tpex serve as a source for the pool of effector T cells, and in the absence of their cognate antigen, they are able to preserve their quantity through a process of self-renewal. However, it remains unknown how TCR engagement impacts the self-renewal capacity of Tpex in settings of continued antigen exposure. Here, we used a Lewis lung carcinoma model that elicits an optimal or attenuated TCR signal in CD8 T cells to investigate its effect on Tpex persistence during tumor development. Longitudinal phenotyping and single-cell transcriptomics of tumor-specific T cells revealed that formation of the Tpex reservoir in tumor-draining lymph nodes, and its subsequent replenishment of intratumoral Tpex, is dependent on optimal TCR engagement. Notably, adoptive transfer of optimally primed Tpex into a tumor setting with attenuated TCR stimulation significantly accelerates their terminal differentiation, contrasting to the sustained self-renewal occuring with optimal TCR stimulation. This TCR-reinforced Tpex development and self-renewal is coupled to proximal positioning to dendritic cell niches and epigenetic imprinting that involves increased chromatin accessibility at Egr2 and Tcf1 target loci. Collectively, our study highlights the critical role of TCR engagement in sustaining Tpex during tumor progression

2024-04-05 | GSE262842 | GEO

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement

Project description:Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement

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Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [WGBS]

Project description:Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [WGBS]

| PRJNA1093469 | ENA

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [scRNAseq]

Project description:Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [scRNAseq]

| PRJNA1093430 | ENA

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [CUT&Tag]

Project description:Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [CUT&Tag]

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Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [WGBS]

2024-04-05 | GSE262843 | GEO

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [scRNAseq]

2024-04-05 | GSE262816 | GEO

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [CUT&Tag]

2024-04-05 | GSE262844 | GEO

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement

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

2024-04-05 | GSE262845 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [ATACseq]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. Flow cytometric and scRNAseq analysis indicated that EGR2 deficient CD8+ T cells had an abnormal effector-like phenotype. To examine whether this was due to epigenetic alterations, we conducted ATACseq analysis on sorted virus-specific tetramer+ CD8+ T cells isolated at day 20 post-infection with chronic LCMV-Cl13 from either littermate control or EGR2 T cell conditional knock-out mice. The resulting data demonstrated that there were substantial epigenetic changes within EGR2 KO CD8+ T cells, suggesting that EGR2 stabilises the exhausted epigenetic state.

2021-03-02 | GSE153136 | GEO

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