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Bulk RNA sequencing of WT and Pim1 -/- bone-marrow-derived myeloid-derived suppressor cells

ABSTRACT: Bulk RNA sequencing of WT and Pim1 -/- bone-marrow-derived myeloid-derived suppressor cells

PROVIDER: PRJNA700415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13648454_1.fastq.gz	Fastqsanger.gz
	SRR13648454_2.fastq.gz	Fastqsanger.gz
	SRR13648455_1.fastq.gz	Fastqsanger.gz
	SRR13648455_2.fastq.gz	Fastqsanger.gz
	SRR13648456_1.fastq.gz	Fastqsanger.gz

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Bulk RNA sequencing of WT and Pim1 -/- bone-marrow-derived myeloid-derived suppressor cells

Project description:There is a strong correlation between myeloid derived suppressor cells (MDSCs) and resistance to immune checkpoint blockade (ICB), but the detailed underlying this correlation are largely unknown. Using single-cell RNA-seq analysis in a bilateral tumor model, we found that immunosuppressive myeloid cells with characteristics of fatty acid oxidative metabolism dominate the immune-cell landscape in ICB-resistant subjects. In addition, we uncovered a previously underappreciated role of a serine/threonine kinase, PIM1, in regulating lipid oxidative metabolism via PPARγ-mediated activities. Enforced PPARγ expression sufficiently rescued metabolic and functional defects of Pim1-/- MDSCs. Consistent with this, pharmacological inhibition of PIM kinase by AZD1208 treatment significantly disrupted myeloid cell–mediated immunosuppression microenvironment and unleashed CD8+ T cell–mediated antitumor immunity, which enhanced PD-L1 blockade in preclinical cancer models. PIM kinase inhibition also sensitized non-responders to PD-L1 blockade by selectively targeting suppressive myeloid cells. Overall, we have identified PIM1 as a metabolic modulator in MDSCs that is associated with ICB resistance and can be therapeutically targeted to overcome ICB resistance.

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