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In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells [ATAC-seq]

ABSTRACT: In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells [ATAC-seq]

PROVIDER: PRJNA847908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19616312_1.fastq.gz	Fastqsanger.gz
	SRR19616312_2.fastq.gz	Fastqsanger.gz
	SRR19616313_1.fastq.gz	Fastqsanger.gz
	SRR19616313_2.fastq.gz	Fastqsanger.gz
	SRR19616314_1.fastq.gz	Fastqsanger.gz

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In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells

Project description:By comparing the multi-omics profile of human NK cells before and after G-CSF in vivo treatment, we identified a pathway that was activated in response to G-CSF treatment, which suppressed IFN-γ secretion in NK cells. Specifically, integrative genomic strategy uncovered that glucocorticoid receptor (GR) was activated and mediated the genomic response to G-CSF treatment in NK cells. Activated GR can inhibit secretion of IFN-γ via promoting interactions between suppressor of cytokine signaling 1 (SOCS1) promoter and enhancer and increase the expression of SOCS1.

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In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells [CUT&TAG]

Project description:Natural killer (NK) cells are lymphocytes of the innate immune system that are involved in controlling tumors or microbial infections through the production of interferon gamma (IFN-γ). Granulocyte-colony stimulating factor (G-CSF) inhibits IFN-γ secretion by NK cells, but the mechanism underlying this effect remains unclear. Here, by comparing the multi-omics profiles of human NK cells before and after in vivo G-CSF treatment, we identified a pathway that was activated in response to G-CSF treatment, which suppressed IFN-γ secretion in NK cells. Specifically, our integrative genomic strategy revealed glucocorticoid receptor (GR) activation in NK cells that mediated the genomic response to G-CSF treatment. Activated GRs can inhibit secretion of IFN-γ by promoting interactions between suppressor of cytokine signaling 1 (SOCS1) promoter and enhancer, as well as increase the expression of SOCS1. Experiments in mice confirmed that G-CSF in vivo treatment significantly down-regulated IFN-γ secretion and up-regulated GR and SOCS1 expression in NK cells. In addition, GR blockade (RU486) significantly reversed the effects of G-CSF, demonstrating that GR up-regulates SOCS1 and inhibits the production of IFN-γ by NK cells.

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