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PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells III.

ABSTRACT: PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells III.

PROVIDER: PRJNA1090866 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28419677_1.fastq.gz	Fastqsanger.gz
	SRR28419677_2.fastq.gz	Fastqsanger.gz
	SRR28419678_1.fastq.gz	Fastqsanger.gz
	SRR28419678_2.fastq.gz	Fastqsanger.gz
	SRR28419679_1.fastq.gz	Fastqsanger.gz

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PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells III.

Project description:Metabolic programming plays a crucial role in T-cell activation. Herein, we describe how phospholipid metabolism regulates CD8+ T-cell function in patients with cancer. We found that phosphatidylcholine (PC) and phosphatidyl ethanolamine (PE) levels were lower in intratumoral CD8+ T cells than in circulating CD8+ T cells. The expression of phospholipid phosphatase 1 (PLPP1), an enzyme that catalyzes PE and PC synthesis, was also downregulated in CD8+ T cells upon infiltrating tumors. Moreover, unsaturated fatty acid-mediated ferroptosis was a major factor impairing the antitumor function of PLPP1-deficient CD8+ T cells infiltrated in tumors, accompanied by enhanced reactive oxygen species production and lipid peroxidation. The activation of programmed cell death 1 (PD-1) signaling in CD8+ T cells suppressed the PLPP1 expression by increasing GATA1 binding to the promoter region of PLPP1. PLPP1 expression was upregulated after anti-PD-1 therapy. Our findings revealed therapeutic potential of enhancing PLPP1 levels to restore CD8+ T-cell function.

2024-05-17 | GSE262231 | GEO

PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells I

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PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells II

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PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells II

Project description:PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells II

| PRJNA1088153 | ENA

PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells I

Project description:PLPP1-deficiency-mediated ferroptosis induced by PD-1 signaling impairs antitumor activity of intratumoral CD8+ T cells I

| PRJNA1088154 | ENA

SERT inhibits CD8 T cell antitumor immunity through regulating the intratumoral serotonin axis

Project description:Identifying new immune checkpoint molecules hindering antitumor T cell responses and devising new therapeutic blockades are key to the development of next-generation cancer immunotherapies. Here, we report the induction of the serotonin transporter (SERT) in solid tumor-infiltrating cytotoxic CD8 T cells, a molecule best known for its role in regulating serotonin neurotransmission in the brain. In solid tumors, CD8 T cells secrete serotonin, which stimulates their antitumor reactivities, while SERT functions as a negative regulator by depleting intratumoral serotonin. Inhibition of SERT using clinically approved selective serotonin reuptake inhibitors (SSRIs), a popular class of antidepressants, significantly suppressed tumor growth and enhanced CD8 T cell-mediated antitumor responses in various preclinical mouse syngeneic and human xenograft tumor models. Importantly, SSRI treatment exhibited significant therapeutic synergy with anti-PD-1 therapy, and clinical data correlation studies negatively associated intratumoral SERT expression with patient survival in a range of cancers. These findings highlight the significance of the intratumoral serotonin axis and identify SERT as a novel immune checkpoint, positioning SSRIs as promising candidates for next-generation combination cancer therapies.

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PLPP1 suppreses breast cancer tumor growth

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CD36-mediated ferroptosis dampens intratumoral CD8<sup>+</sup> T cell effector function and impairs their antitumor ability.

Project description:Understanding the mechanisms underlying how T cells become dysfunctional in a tumor microenvironment (TME) will greatly benefit cancer immunotherapy. We found that increased CD36 expression in tumor-infiltrating CD8+ T cells, which was induced by TME cholesterol, was associated with tumor progression and poor survival in human and murine cancers. Genetic ablation of Cd36 in effector CD8+ T cells exhibited increased cytotoxic cytokine production and enhanced tumor eradication. CD36 mediated uptake of fatty acids by tumor-infiltrating CD8+ T cells in TME, induced lipid peroxidation and ferroptosis, and led to reduced cytotoxic cytokine production and impaired antitumor ability. Blocking CD36 or inhibiting ferroptosis in CD8+ T cells effectively restored their antitumor activity and, more importantly, possessed greater antitumor efficacy in combination with anti-PD-1 antibodies. This study reveals a new mechanism of CD36 regulating the function of CD8+ effector T cells and therapeutic potential of targeting CD36 or inhibiting ferroptosis to restore T cell function.

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