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An oncolytic virus–delivered TGFβ inhibitor overcomes the immunosuppressive tumor microenvironment

ABSTRACT: An oncolytic virus–delivered TGFβ inhibitor overcomes the immunosuppressive tumor microenvironment

PROVIDER: PRJNA779090 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16893573_1.fastq.gz	Fastqsanger.gz
	SRR16893573_2.fastq.gz	Fastqsanger.gz
	SRR16893574_1.fastq.gz	Fastqsanger.gz
	SRR16893574_2.fastq.gz	Fastqsanger.gz
	SRR16893575_1.fastq.gz	Fastqsanger.gz

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An oncolytic virus–delivered TGFβ inhibitor overcomes the immunosuppressive tumor microenvironment

Project description:Oncolytic viruses (OV) are promising forms of immunotherapy that have demonstrated clinical benefit in difficult-to-treat cancers such as metastatic melanoma. However, their adoption in other malignancies has been limited, in part, due to poorly understood mechansims of therapeutic resistance. Here, bulk RNA-seq was performed on oncolytic vaccinia virus-sensitive and -resistant murine head and neck squamous cell carcinomas (MEERvvS and MEERvvR, respectively) to explore potential means of OV resistance. These results corroborated a potential role for TGF-beta mediated stabilization of immunosuppressive regulatory T cells in the tumor microenvironment of OV-resistant MEERvvR-bearing mice. Subsequently, treatment with oncolytic vaccinia virus engineered to expess a dominant negative TGF-β signaling inhibitor (VVtgfbi) restored sensitivity to OV-mediated cell death among MEERvvR tumors. Single-cell RNA seq performed on CD45+ immune cells isolated from tumors suggests TGF-β inhibition may also reduce the presence and activity of myeloid-derived suppressor cell populations within the tumor microenvironment.

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Project description:Oncolytic viruses are promising immunotherapeutic agents, but their efficacy, particularly following intra-tumoural injection, in relation to the size of the targeted tumour, is unclear. Here we show that an oncolytic rhabdovirus, maraba, activates an immune response in human as well as mouse pre-clinical systems, which targets viral as well as tumour-associated antigens. The addition of immune checkpoint blockade to virotherapy is apparent only on the treatment of larger tumours, which have an inherently more immunosuppressive tumour microenvironment, including skewing of T cell receptor engagement with antigen from conventional to regulatory CD4+ cells. Maraba converts the immunologically cold tumour to hot, thus priming the tumour microenvironment for effective αPD1 combination therapy. This study supports the use of maraba oncolytic virotherapy in combination with immune checkpoint inhibitors in melanoma and highlights the impact of the tumour burden on the immune microenvironment and benefit of single agent and combination treatment.

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