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SMART-seq of PD1+ and PD1- CD8 T cells derived from Setx L389S (Setx KI) mice

ABSTRACT: SMART-seq of PD1+ and PD1- CD8 T cells derived from Setx L389S (Setx KI) mice

PROVIDER: PRJNA821103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18516727_1.fastq.gz	Fastqsanger.gz
	SRR18516727_2.fastq.gz	Fastqsanger.gz
	SRR18516728_1.fastq.gz	Fastqsanger.gz
	SRR18516728_2.fastq.gz	Fastqsanger.gz
	SRR18516729_1.fastq.gz	Fastqsanger.gz

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SMART-seq of PD1+ and PD1- CD8 T cells derived from Setx L389S (Setx KI) mice

Project description:The goal is to understand the nature of PD-1+ CD8 T cells that are detected in the peripheral blood of ALS4 mice (expressing the mutation SetxL389S, also called Setx KI mice). We performed a SMART (Switching Mechanism At the end of the 5’-end of the RNA Transcript)-sequencing analysis of the transcriptome of effector memory CD8 T cells expressing or not PD-1 from the blood of symptomatic KI animals. Amongst the transcripts differentially expressed between these two populations, we detected upregulation of Tox (Thymocyte Selection Associated High Mobility Group Box) in PD-1+ as compared to PD-1- CD8 T cells.

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RNA-seq of Setx KI and WT Spinal Cord

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Project description:PD-1 blockade therapy, harnessing the cytotoxic potential of CD8+ T cells, has yielded clinical success in treating malignancies. However, its efficacy is often limited due to the progressive differentiation of intratumoral CD8+ T cells into a hypofunctional state known as terminal exhaustion. Despite identifying CD8+ T cell subsets associated with immunotherapy resistance, the molecular pathway triggering the resistance remains elusive. Given the clear association of CD38 with CD8+ T cell subsets resistant to anti-PD1 therapy, we investigated its role in inducing resistance. Phenotypic and functional characterization, along with single-cell RNA sequencing analysis of both in vitro chronically stimulated and intratumoral CD8+ T cells, revealed that CD38-expressing CD8+ T cells are terminally exhausted. Exploring the molecular mechanism, we discovered that CD38 expression was crucial in promoting terminal differentiation of CD8+ T cells by suppressing TCF1 expression, thereby rendering them unresponsive to anti-PD1 therapy. Genetic ablation of CD38 in tumor reactive CD8+ T cells restored TCF1 levels and improved the responsiveness to anti-PD1 therapy in mice. Mechanistically, CD38 expression on exhausted CD8+ T cells elevated intracellular Ca2+ levels through RyR2 calcium channel activation. This, in turn, promoted chronic AKT activation, leading to TCF1 loss. Knockdown of RyR2 or inhibition of AKT in CD8+ T cells maintained TCF1 levels, induced a sustained anti-tumor response, and enhanced responsiveness to anti-PD1 therapy. Thus, targeting CD38 represents a potential strategy to improve the efficacy of anti-PD1 treatment in cancer.

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