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RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumor immunity

ABSTRACT: RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumor immunity

PROVIDER: PRJNA957281 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24210806_1.fastq.gz	Fastqsanger.gz
	SRR24210806_2.fastq.gz	Fastqsanger.gz
	SRR24210807_1.fastq.gz	Fastqsanger.gz
	SRR24210807_2.fastq.gz	Fastqsanger.gz
	SRR24210808_1.fastq.gz	Fastqsanger.gz

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RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumor immunity

Project description:RIG-I is a pattern recognition receptor involved in innate immunity, but its role in adaptive immunity remains unclear. Here, we demonstrate that RIG-I is upregulated in tumor infiltrating CD8+ T cells, where it functions as an intracellular checkpoint to negatively regulate CD8+ T cell function and limit antitumor immunity. Mechanically, up-regulation of RIG-I in CD8+ T cells is induced by retinoic acid (RA), a metabolite of vitamin A in TME, and direct inhibits the AKT/glycolysis signaling pathway. In addition, deletion of RIG-I enhances the efficacy of adoptively transferred T cells against solid tumors and inhibition of RIG-I enhances the response to PD-1 blockade. Our findings identify RIG-I as an intracellular checkpoint and a potential target for alleviating inhibitory constraints on T cells in cancer immunotherapy, either alone or in combination with immune checkpoint blockade.

2023-04-25 | GSE230045 | GEO

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Project description:RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumor immunity

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UBE2D3 is an Intracellular Checkpoint in Pancreatic Ductal Carcinoma that Restricts CD8+ T-Cell Antitumor Immunity

Project description:UBE2D3 is an Intracellular Checkpoint in Pancreatic Ductal Carcinoma that Restricts CD8+ T-Cell Antitumor Immunity

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UBE2D3 is an Intracellular Checkpoint in Pancreatic Ductal Carcinoma that Restricts CD8+ T-Cell Antitumor Immunity II

Project description:UBE2D3 is an Intracellular Checkpoint in Pancreatic Ductal Carcinoma that Restricts CD8+ T-Cell Antitumor Immunity II

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RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumour immunity

Project description: Not available

| S-BSST1481 | biostudies-other

RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumour immunity

Project description: Not available

| S-BSST1473 | biostudies-other

RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumour immunity

Project description: Not available

| S-BSST1468 | biostudies-other

RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumour immunity

Project description:Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor involved in innate immunity, but its role in adaptive immunity, specifically in the context of CD8+ T-cell antitumour immunity, remains unclear. Here, we demonstrate that RIG-I is upregulated in tumour-infiltrating CD8+ T cells, where it functions as an intracellular checkpoint to negatively regulate CD8+ T-cell function and limit antitumour immunity. Mechanistically, the upregulation of RIG-I in CD8+ T cells is induced by activated T cells, and directly inhibits the AKT/glycolysis signalling pathway. In addition, knocking out RIG-I enhances the efficacy of adoptively transferred T cells against solid tumours, and inhibiting RIG-I enhances the response to PD-1 blockade. Overall, our study identifies RIG-I as an intracellular checkpoint and a potential target for alleviating inhibitory constraints on T cells in cancer immunotherapy, either alone or in combination with an immune checkpoint inhibitor.

| S-SCDT-10_1038-S44321-024-00136-9 | biostudies-other

STUB1 is an intracellular checkpoint for interferon gamma sensing

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PTP1B Is an Intracellular Checkpoint that Limits T-cell and CAR T-cell Antitumor Immunity.

Project description:Immunotherapies aimed at alleviating the inhibitory constraints on T cells have revolutionized cancer management. To date, these have focused on the blockade of cell-surface checkpoints such as PD-1. Herein we identify protein tyrosine phosphatase 1B (PTP1B) as an intracellular checkpoint that is upregulated in T cells in tumors. We show that increased PTP1B limits T-cell expansion and cytotoxicity to contribute to tumor growth. T cell-specific PTP1B deletion increased STAT5 signaling, and this enhanced the antigen-induced expansion and cytotoxicity of CD8+ T cells to suppress tumor growth. The pharmacologic inhibition of PTP1B recapitulated the T cell-mediated repression of tumor growth and enhanced the response to PD-1 blockade. Furthermore, the deletion or inhibition of PTP1B enhanced the efficacy of adoptively transferred chimeric antigen receptor (CAR) T cells against solid tumors. Our findings identify PTP1B as an intracellular checkpoint whose inhibition can alleviate the inhibitory constraints on T cells and CAR T cells to combat cancer.SignificanceTumors subvert antitumor immunity by engaging checkpoints that promote T-cell exhaustion. Here we identify PTP1B as an intracellular checkpoint and therapeutic target. We show that PTP1B is upregulated in intratumoral T cells and that its deletion or inhibition enhances T-cell antitumor activity and increases CAR T-cell effectiveness against solid tumors. This article is highlighted in the In This Issue feature, p. 587.

| S-EPMC8904293 | biostudies-literature

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