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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: PRJNA590272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13439043.fastq.gz	Fastqsanger.gz
	SRR13439044.fastq.gz	Fastqsanger.gz
	SRR13439045.fastq.gz	Fastqsanger.gz
	SRR13439046.fastq.gz	Fastqsanger.gz
	SRR13439047.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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Sox4 links tumor suppression to accelerated aging in mice

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Proteomic assessments of muscle tissues in cattle that are diet restricted and subsequently undergo compensatory growth

Project description:Compensatory growth is a naturally occurring accelerated growth phenomenon observed in cattle upon re-alimentation following a prior period of dietary restriction (Hornick et al., 2000). It is incorporated into man production systems as a method to reduce feed costs and consequently is economically important for animal production systems. The goal of our research project is to identify biomarkers for cattle with a superior ability to display compensatory growth. Transcriptional profiling studies of liver and muscle tissues in cattle have shown large numbers of differentially expressed genes in animals undergoing dietary restriction and subsequent compensatory growth when compared to a continuously-fed ad libitum control group of cattle (Connor et al., 2010; Keogh et al., 2016a,b). Given the identification of differential expression at the transcript level, the intended project aims to evaluate potential differences in protein abundance between animals that are diet restricted and subsequently undergo compensatory growth compared to a continuously-fed ad libitum control group of cattle. Differences in genes that are apparent at both the protein and the transcript level are more likely to be transferable across breed type (Snelling et al., 2013) and consequently have more utility for incorporation within genomic selection breeding programs for cattle evaluations.

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Project description:Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis.

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2023-01-13 | GSE165285 | GEO

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