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ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

ABSTRACT: ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

PROVIDER: PRJNA991595 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25152360_1.fastq.gz	Fastqsanger.gz
	SRR25152360_2.fastq.gz	Fastqsanger.gz
	SRR25152361_1.fastq.gz	Fastqsanger.gz
	SRR25152361_2.fastq.gz	Fastqsanger.gz
	SRR25152362_1.fastq.gz	Fastqsanger.gz

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ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

Project description:CD8+ T cell immune responses are regulated by multi-layer networks, while the post-translational regulations remain largely unknown. Transmembrane ectodomain shedding is an important post-translational process regulating receptor expression and signal transduction by proteolytic cleavage of membrane proteins. Here, by targeting sheddase A Disintegrin and Metalloprotease (ADAM)17, we defined a post-translational regulatory mechanism mediated by ectodomain shedding in CD8+ T cells. Transcriptomic and proteomic analysis revealed the involvement of post-transcriptional/translational regulations in CD8+ T cells. T cell-specific deletion of ADAM17 led to a dramatic increase of effector CD8+ T cell differentiation and enhanced cytolytic effects to eliminate pathogens and tumors. Mechanistically, ADAM17 regulated CD8+ T cells by cleavage of membrane CD122. ADAM17 deficient CD8+ T cells had elevated CD122 expression and response to cytokines IL-2 and IL-15. Intriguingly, inhibition of ADAM17 in CD8+ T cells improved the efficacy of chimeric antigen receptor (CAR) T cells in solid tumor. Our findings reveal a critical post-translational regulation in CD8+ T cells, providing a potential therapeutic strategy of targeting ADAM17 for effective anti-tumor immunity. We then performed gene expression profiling analysis using data obtained from RNA-seq of 10 samples from two groups.

2024-07-20 | GSE236582 | GEO

Expression data from Adam17 knock out mice and wild type

Project description:Adam17, a shedding protease, is strongly upregtulated during inflammation and cancer. Here we investigate the genome wide effects of Adam17 knock out on the transcriptome. Mouse tissue samples from n=3 wildtype colon, n=3 Adam17 knockout colon, n=3 wildtype skin and n=3 Adam17 knockout skin were used in the study.

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Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

Project description:This study investigates the role of ADAM17 (a disintegrin and metalloproteinase 17) in skin homeostasis. Here, we show that mice lacking ADAM17 in keratinocytes have a normal epidermal barrier and skin architecture at birth, but develop pronounced defects in epidermal barrier integrity soon after birth and chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 days after birth, followed by transepidermal water loss and inflammatory immune cell infiltration. Our results identify a previously unappreciated critical role of the ADAM17/EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier. The genome-wide effects of ADAM17 deficiency were analyzed using Agilent Whole Mouse Genome microarrays. Conditional keratinocyte-specific ADAM17 knockout mice were generated by crossing Adam17flox/flox mice with keratin-14-Cre (Krt14-Cre) transgenic mice. Adam17flox/+Krt14-Cre mice were mated with Adam17flox/flox mice to generate pups of Adam17flox/flox Krt14-Cre positive (cKO) and Krt14-Cre negative (wild-type) control littermates. The genetic background was a mix of 129Sv and C57BL/6. As material, back skin tissue biopsies (postnatal day 10) from n = 2 wild-type skin and n = 2 ADAM17 epidermal KO skin (matched WT-cKO pairs from two different litters) were used in this study.

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Next Generation Sequencing of skin from wild-type and ADAM17 cKO (Sox9-Cre x ADAM17fl/fl) mice

Project description:Purpose: Transcriptomic analysis of ADAM17 cKO mice, a mouse model of atopic dermatitis. Methods: Skin was harvested from 10-week-old wild-type and ADAM17 cKO mice and were subjected to next generation sequencing as described. Results: Of 13,573 genes analyzed by GSA, 2514 differentially expressed genes (DEGs) were detected in ADAM17 cKO skin using a standard definition including both statistically significant change (P-value < 0.01; FDR < 0.05) and effect size (|fold change| > 2) . These DEGs included genes important in lipid metabolism and keratinization, consistent with the understanding of barrier dysfunction in atopic inflammation, as well as significant immunologic pathways in adaptive and innate immunity previously identified in the human AD transcriptome Conclusions: Our study reveals that the transcriptome of ADAM17 cKO mice capture a part of upregulated genes previously observed in human AD skin.

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FTO degradation targeting enhances anti-tumor immunity

Project description:FTO degradation targeting enhances anti-tumor immunity

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Project description:Acute and chronic pancreatitis, the latter associated with fibrosis, are multifactorial inflammatory disorders and leading causes of gastrointestinal disease-related hospitalisation, including death. Despite the global health burden of pancreatitis, currently there are no effective therapeutic agents. In this regard, the protease A Disintegrin And Metalloproteinase 17 (ADAM17) mediates inflammatory responses through shedding of bioactive inflammatory cytokines and mediators, including tumour necrosis factor α (TNFα) and the soluble interleukin (IL)-6 receptor (sIL-6R), the latter of which drives proinflammatory IL-6 trans-signalling. However, the role of ADAM17 in pancreatitis is unclear. To address this, Adam17ex/ex mice – which are homozygous for the hypomorphic Adam17ex allele resulting in marked reduction in ADAM17 expression – and their wild-type (WT) littermates were exposed to the cerulein-induced acute pancreatitis model, and acute (1-week) and chronic (20-weeks) pancreatitis models induced by the cigarette smoke carcinogen nicotine-derived nitrosamine ketone (NNK). Our data reveal that ADAM17 expression was upregulated in pancreatic tissues of animal models of pancreatitis. Moreover, the genetic (Adam17ex/ex mice) and therapeutic (ADAM17 prodomain inhibitor; A17pro) targeting of ADAM17 ameliorated experimental pancreatitis, which was associated with a reduction in the IL-6 trans-signalling/STAT3 axis. This led to reduced inflammatory cell infiltration, including T cells and neutrophils, as well as necrosis and fibrosis in the pancreas. Furthermore, upregulation of the ADAM17/IL-6 trans-signalling/STAT3 axis was a feature of pancreatitis patients. Collectively, our findings indicate that the ADAM17 protease plays a pivotal role in the pathogenesis of pancreatitis, which could pave the way for devising novel therapeutic options to be deployed against this disease.

2022-10-06 | GSE214666 | GEO

eIF4A1 enhances LARP1-mediated translational repression during mTORC1 inhibition

Project description:eIF4A1 enhances LARP1-mediated translational repression during mTORC1 inhibition

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Expression data from Adam17 knock out mice and wild type

Project description:Adam17, a shedding protease, is strongly upregtulated during inflammation and cancer. Here we investigate the genome wide effects of Adam17 knock out on the transcriptome.

2010-06-18 | GSE21691 | GEO

BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity

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