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Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

ABSTRACT: Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

PROVIDER: PRJNA917641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22959454_1.fastq.gz	Fastqsanger.gz
	SRR22959454_2.fastq.gz	Fastqsanger.gz
	SRR22959455_1.fastq.gz	Fastqsanger.gz
	SRR22959455_2.fastq.gz	Fastqsanger.gz
	SRR22959456_1.fastq.gz	Fastqsanger.gz

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Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

Project description:Although promising, dendritic cell (DC) vaccines still provide limited clinical benefits, mainly due to the immunosuppressive tumor microenvironment (TME) and the lack of tumor-associated antigens (TAAs). Oncolytic viruses are considered to be an ideal strategy to overcome immunosuppression and expose TAAs, therefore they may work synergistically with DC vaccines. In this study, we demonstrated that oncolytic virus M1 (OVM) can enhance the antitumor effects of DC vaccine in a variety of syngeneic tumor mouse models by increasing the infiltration of CD8+ effector T cells in the TME. Mechanically, we identified that tumor cells offset the function of DC vaccines through the myeloid immune checkpoint SIRPα-CD47, while OVM can downregulate the expression of SIRPα and CD47 in DCs and tumor cells, respectively. Based on the fact that OVM upregulates the expression of PD-L1 in DCs, PD-L1 blockade was introduced with the combination of DC vaccines and OVM, resulting in a further potentiation of antitumor activity. Overall, we revealed that OVM can strengthen the antitumor efficacy of DC vaccines by targeting the immune checkpoint SIRPα-CD47 axis, which exerts dominant immunosuppressive effects on DC vaccines.

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Project description:Gene set enrichment analysis (GSEA) revealed that upon M1 treatment, apoptotic and inflammation associated genes were largely upregulated, suggesting that M1 killed tumor cells and triggered inflammatory response. The GSEA also revealed that DNA repair pathway was down-regulated in M1 treated tumors, which is consistent with our previous finding that M1 induces DNA damage and then leads to tumor cells apoptosis. Additionally, gene sets marked the release of immune-boosting cytokines such as interferon (IFN)-α, IFN-γand tumor necrosis factor (TNF)-α were deployed in M1 treated tumors, providing potential pro-inflammatory signals to generate antitumor immunity. All the results above demonstrate that M1 induces ICD and shapes TME to an inflammatory state.

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Intravenous injection of oncolytic virus M1 awakes antitumor T cells and overcomes resistance to checkpoint blockade

Project description:Intravenous injection of oncolytic virus M1 awakes antitumor T cells and overcomes resistance to checkpoint blockade

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