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Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

ABSTRACT: Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

PROVIDER: PRJNA528597 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8768153_1.fastq.gz	Fastqsanger.gz
	SRR8768153_2.fastq.gz	Fastqsanger.gz
	SRR8768154_1.fastq.gz	Fastqsanger.gz
	SRR8768154_2.fastq.gz	Fastqsanger.gz
	SRR8768155_1.fastq.gz	Fastqsanger.gz

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Regulatory T Cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis

Project description:Regulatory T Cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis

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Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

Project description:Regulatory T cells (Treg) are common in the tumor microenvironment in both human pancreatic cancer and in genetically engineered mouse models of the disease. Previous studies in orthotopic syngeneic models of pancreatic cancer -recapitulated in our own data- indicated that Treg depletion results CD8+ T cell-mediated tumor regression. In human patients and in mouse models, regulatory T cells accumulate during the onset of Pancreatic Intraepithelial Neoplasia (PanIN), the earliest steps of carcinogenesis. We thus generated a genetic model to investigate the role of regulatory T cells during the onset of pancreatic carcinogenesis. Unexpectedly, depletion of Tregs during early stages of carcinogenesis led to accelerated tumor progression.

2019-03-23 | GSE128707 | GEO

Regulatory T Cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis

Project description:In human patients and in mouse models, immunosuppressive regulatory T cells(Tregs)accumulate in Pancreatic Intraepithelial Neoplasia (PanIN), the precursor lesions to pancreatic cancer. Tregs are considered a potential therapeutic target with the goal to reverse immunosuppression in a number of malignancies, including pancreatic cancer. Here, using a genetically engineered mouse that allows at will depletion of Tregs during pancreatic carcinogenesis, we determined that Treg depletion failed to relieve immunosuppression. Contradicting the current paradigm, depletion of Tregs led to accelerated tumorprogression. We demonstratedthat Treg depletion resultsin changes in the fibroblast population, exemplified by loss of Smooth Muscle Actinexpression and an increase the myeloid recruiting chemokines Ccl3, Ccl6, and Ccl8. Treg depletion further resulted ina compensatoryinflux of suppressive myeloid cells, thereby preventing an anti-tumor immune response. Mechanistically, we show that themyeloid recruitment was driven through the CCR1 axis, with the receptor expressed on tumor associated myeloid cells and several ligands up-regulated in epithelial cells and fibroblasts upon Treg depletion. Finally,blockade of CCR1 signalingcombined with Treg-depletionsuccessfully inhibitedtumorigenesis, uncovering the immune-suppressive myeloid CCR1 axis as a potential therapeutic targetin pancreatic cancer.

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