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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

ABSTRACT: Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

PROVIDER: PRJNA547551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12024202_1.fastq.gz	Fastqsanger.gz
	SRR12024202_2.fastq.gz	Fastqsanger.gz
	SRR12024203_1.fastq.gz	Fastqsanger.gz
	SRR12024203_2.fastq.gz	Fastqsanger.gz
	SRR12024204_1.fastq.gz	Fastqsanger.gz

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [mouse]

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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

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Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

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The efficacy of chemotherapy is limited by intratumoral senescent cells that persist through the upregulation of PD-L2

Project description:Anti-cancer therapies often result in a subset of surviving cancer cells that undergo therapy induced senescence (TIS). Senescent cancer cells strongly modify the intratumoral microenvironment favoring immunosuppression and, thereby, tumor growth. An emerging strategy to optimise current therapies is to combine them with treatments that eliminate senescent cells. To this end, we undertook an unbiased proteomics approach to identify surface markers contributing to senescent cells immune evasion. Through this approach, we discovered that the immune checkpoint inhibitor PD-L2, but not PD-L1, is upregulated across multiple senescent human and murine cells. Importantly, blockade of PD-L2 strongly synergises with genotoxic chemotherapy, causing remission of solid tumors in mice. We show that PD-L2 inhibition prevents the persistence of chemotherapy-induced senescent cells, which exert cell-extrinsic immunomodulatory actions. In particular, upon chemotherapy, tumors deficient in PD-L2 fail to produce cytokines of the CXCL family, do not recruit myeloid-derived suppressor cells (MDSCs) and are eliminated in a CD8 T cell-dependent manner. We conclude that blockade of PD-L2 improves chemotherapy efficacy by reducing the intratumoral burden of senescent cells and their associated recruitment of immunosuppressive cells. These findings provide a novel strategy to exploit vulnerabilities arising in tumor cells as a result of therapy-induced damage and cellular senescence

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Intratumoral follicular regulatory T cells curtail anti-PD-1 treatment efficacy.

Project description:Immune-checkpoint blockade (ICB) has shown remarkable clinical success in boosting antitumor immunity. However, the breadth of its cellular targets and specific mode of action remain elusive. We find that tumor-infiltrating follicular regulatory T (TFR) cells are prevalent in tumor tissues of several cancer types. They are primarily located within tertiary lymphoid structures and exhibit superior suppressive capacity and in vivo persistence as compared with regulatory T cells, with which they share a clonal and developmental relationship. In syngeneic tumor models, anti-PD-1 treatment increases the number of tumor-infiltrating TFR cells. Both TFR cell deficiency and the depletion of TFR cells with anti-CTLA-4 before anti-PD-1 treatment improve tumor control in mice. Notably, in a cohort of 271 patients with melanoma, treatment with anti-CTLA-4 followed by anti-PD-1 at progression was associated with better a survival outcome than monotherapy with anti-PD-1 or anti-CTLA-4, anti-PD-1 followed by anti-CTLA-4 at progression or concomitant combination therapy.

| S-EPMC8434898 | biostudies-literature

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