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STING agonist alters the transcriptional profiles of HSPCs in melanoma-bearing mouse model

ABSTRACT: STING agonist alters the transcriptional profiles of HSPCs in melanoma-bearing mouse model

PROVIDER: PRJNA793834 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17409771_1.fastq.gz	Fastqsanger.gz
	SRR17409771_2.fastq.gz	Fastqsanger.gz
	SRR17409772_1.fastq.gz	Fastqsanger.gz
	SRR17409772_2.fastq.gz	Fastqsanger.gz
	SRR17409773_1.fastq.gz	Fastqsanger.gz

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STING agonist alters the transcriptional profiles of HSPCs in melanoma-bearing mouse model

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Transcriptome-wide identification of STING agonist programed B cells

Project description:We employed RNA-seq to study the transcriptomic change in B lymphocytes in response to STING agonist. Transcriptomic analysis of wild type and TMEM173–/– B cells stimulated with STING agonist revealed that the inflammatory response pathway enriched in 3'3'-cGAMP treated WT B cells but lacking in Tmem173-/-B cells comprised of a cluster containing inhibitory regulators, provoking STING signal to evade immune surveillance by inducing an immunosuppressive B cell population.

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Transcriptome-wide identification of STING agonist programed B cells

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Project description:Upon systemic bacterial infection, hematopoietic stem and progenitor cells (HSPCs) migrate to the periphery in order to supply a sufficient number of immune cells. Although pathogen-associated molecular patterns (PAMPs) reportedly mediate HSPC activation, how HSPCs detect pathogen invasion in vivo remains elusive. Bacteria use the second messenger bis-(3’-5’)-cyclic dimeric guanosine monophosphate (c-di-GMP) for a variety of activities. Here we report that c-di-GMP comprehensively regulates both HSPCs and their niche cells through an innate immune sensor, STING, thereby inducing entry into the cell cycle and mobilization of HSPCs, while decreasing the number and repopulation capacity of long-term hematopoietic stem cells (LT-HSCs). Furthermore, we show that type I IFN acts as a downstream target of c-di-GMP to inhibit HSPC expansion in the spleen, while TGF-β1 is required for c-di-GMP-dependent splenic HSPC expansion. Our results define novel machinery underlying dynamic regulation of HSPCs and their niches during bacterial infection through c-di-GMP/STING signaling. Ten-week-old mice were intraperitoneally administered PBS or 200 nmol c-di-GMP, and CD150+ CD41- CD48- CD34- Flt3- LSK cells of pooled bone marrow from 10 mice per group were sorted 3 days later. mRNA was then extracted using RNeasy micro (Qiagen). Likewise, CD45- Ter-119- CD31- CD140a+ CD51+ MSCs and CD45- Ter119- CD31+ endothelial cells from c-di-GMP-treated or untreated mice were sorted and mRNA was extracted. cDNA was synthesized from mRNA and hybridized to gene chip Mouse60k (Agilent Technologies) and expression levels analyzed.

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