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Macrophage-targeted Therapy Unlocks Antitumoral Crosstalk Between IFN휸-secreting Lymphocytes and IL12-producing Dendritic Cells

ABSTRACT: Macrophage-targeted Therapy Unlocks Antitumoral Crosstalk Between IFN휸-secreting Lymphocytes and IL12-producing Dendritic Cells

PROVIDER: PRJNA679323 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13082456_1.fastq.gz	Fastqsanger.gz
	SRR13082456_2.fastq.gz	Fastqsanger.gz
	SRR13082457.fastq.gz	Fastqsanger.gz
	SRR13082458_1.fastq.gz	Fastqsanger.gz
	SRR13082458_2.fastq.gz	Fastqsanger.gz

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Macrophage-targeted Therapy Unlocks Antitumoral Crosstalk Between IFN -secreting Lymphocytes and IL12-producing Dendritic Cells

Project description:Macrophages often abound within tumors, express colony-stimulating factor 1 receptor (CSF1R), and are linked to adverse patient survival. Drugs blocking CSF1R signaling have been used to suppress tumor-promoting macrophage responses; however, their mechanisms of action remain incompletely understood. Here, we assessed the lung tumor immune microenvironment in mice treated with BLZ945, a prototypical small-molecule CSF1R inhibitor, using single-cell RNA sequencing and mechanistic validation approaches. We showed that tumor control was not caused by CSF1R+ cell depletion; instead, CSF1R targeting reshaped the CSF1R+ cell landscape, which unlocked crosstalk between antitumoral CSF1R- cells. These cells included IFN -producing natural killer and T cells, and an IL12-producing dendritic cell subset, denoted as DC3, which were all necessary for CSF1R inhibitor–mediated lung tumor control. These data indicate that CSF1R targeting can activate a cardinal crosstalk between cells that are not macrophages and that are essential to mediate the effects of T cell–targeted immunotherapies and promote antitumor immunity.

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Macrophage-Targeted Therapy Unlocks Antitumoral Cross-talk between IFNγ-Secreting Lymphocytes and IL12-Producing Dendritic Cells.

Project description:Macrophages often abound within tumors, express colony-stimulating factor 1 receptor (CSF1R), and are linked to adverse patient survival. Drugs blocking CSF1R signaling have been used to suppress tumor-promoting macrophage responses; however, their mechanisms of action remain incompletely understood. Here, we assessed the lung tumor immune microenvironment in mice treated with BLZ945, a prototypical small-molecule CSF1R inhibitor, using single-cell RNA sequencing and mechanistic validation approaches. We showed that tumor control was not caused by CSF1R+ cell depletion; instead, CSF1R targeting reshaped the CSF1R+ cell landscape, which unlocked cross-talk between antitumoral CSF1R- cells. These cells included IFNγ-producing natural killer and T cells, and an IL12-producing dendritic cell subset, denoted as DC3, which were all necessary for CSF1R inhibitor-mediated lung tumor control. These data indicate that CSF1R targeting can activate a cardinal cross-talk between cells that are not macrophages and that are essential to mediate the effects of T cell-targeted immunotherapies and promote antitumor immunity.See related Spotlight by Burrello and de Visser, p. 4.

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