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Single cell transcriptomics of several organs in K14HPV16/H2b and FVBN/H2b mice.

ABSTRACT: Single cell transcriptomics of several organs in K14HPV16/H2b and FVBN/H2b mice.

PROVIDER: PRJNA1010861 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25819911_1.fastq.gz	Fastqsanger.gz
	SRR25819911_2.fastq.gz	Fastqsanger.gz
	SRR25819912_1.fastq.gz	Fastqsanger.gz
	SRR25819912_2.fastq.gz	Fastqsanger.gz
	SRR25819913_1.fastq.gz	Fastqsanger.gz

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Single cell transcriptomics of several organs in K14HPV16/H2b and FVBN/H2b mice.

Project description:It is well established that symptomatic cancers evade immune destruction by coalescing lesional and tumor microenvironments to suppress adaptive immunity. Additionally, mouse models of cervical and other cancers have revealed a capability of tumors to systemically induce the expansion of myeloid cells that cripple T cell development in spleen and lymph nodes, further impairing immune responses. We show that HPV16-driven cervical cancers release into the circulatory system four immunoregulatory ligands – IL1α, IL1ß, IL33, and IL36ß – that bias the bone marrow toward granulocytic myelopoiesis, producing immunosuppressive neutrophils and myeloid progenitors differentially populating spleens and tumors to facilitate immune evasion. A pan-IL1 receptor antagonist, anti-IL1RAP, attenuates this myeloid expansion and complements an HPV-E7 peptide vaccine plus anti-CTLA4 to elicit anti-tumor immunity. Evidence for similar systemic activity of these four IL1 ligands in human cervical and other cancers encourages multi-targeting this signaling axis to broaden the scope of cancer immunotherapy.

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