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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

ABSTRACT: Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

PROVIDER: PRJNA807345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18042400_1.fastq.gz	Fastqsanger.gz
	SRR18042400_2.fastq.gz	Fastqsanger.gz
	SRR18042401_1.fastq.gz	Fastqsanger.gz
	SRR18042401_2.fastq.gz	Fastqsanger.gz
	SRR18042402_1.fastq.gz	Fastqsanger.gz

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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

Project description:Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

| PRJNA807349 | ENA

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [HMC-1]

Project description:Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [HMC-1]

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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer.

Project description:BackgroundPreviously, we uncovered a patient subgroup with highly malignant pancreatic cancer with serum markers CEA+/CA125+/CA19-9 ≥ 1000 U/mL (triple-positive, TP). However, the underlying immunosuppressive mechanism in the tumor immune microenvironment (TIME) of this subgroup is still unknown.MethodsHuman tissues were analyzed by flow cytometry, mass cytometry, and immunofluorescence staining. Mouse pancreatic ILC2s were expanded in vivo and used for RNA sequencing, chromatin immunoprecipitation (ChIP), and chemotaxis assays.FindingsThrough microarray data, we identified the accumulation of the hypoxia-induced factor-1α (HIF-1α) pathway in these TP patients. Via flow and mass cytometry, we discovered that a special subset of ILC2s were highly infiltrated in TP patients. Under the hypoxia microenvironment, ILC2s were found undergo a transition to a IL10+ regulatory phenotype, we named ILCregs which was correlated with pancreatic ductal adenocarcinoma (PDAC) progression. Further, neoadjuvant chemotherapy could ameliorate hypoxic tumor microenvironments so that significantly reverse the regulatory phenotype of ILCregs. Moreover, most tumor ILC2 were CD103-, which indicated its circulatory origin. The expression of Ccr2 was significantly upregulated on mouse ILCregs, and these cells selectively migrated to CCL2.InterpretationOur results indicate that the hypoxia microenvironment creates an immunosuppressive TIME by inducing ILCregs from a population of circulating group 2 ILCs in TP PDAC patients.FundingThis study was jointly supported by the National Natural Science Foundation of China (U21A20374, 82173091, and 81701630).

| S-EPMC9117270 | biostudies-literature

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

Project description:ILC2 cells from mice cultured with or without hypoxia for indicated time period were analysed

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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [HMC-1]

Project description:Humans mast cell line-1 (HMC-1) cultured with or without hypoxia for indicated time period were analysed

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Group-2 Innate Lymphoid Cells Promote Hepatocellular Carcinoma Progression via CXCL2-Neutrophil Induced Immunosuppression

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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

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