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Quantitative Transcriptome Analysis of T cells stimulated with STING ligands

ABSTRACT: Quantitative Transcriptome Analysis of T cells stimulated with STING ligands

PROVIDER: PRJNA413658 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6148730.fastq.gz	Fastqsanger.gz
	SRR6148731.fastq.gz	Fastqsanger.gz
	SRR6148732.fastq.gz	Fastqsanger.gz
	SRR6148733.fastq.gz	Fastqsanger.gz
	SRR6148724.fastq.gz	Fastqsanger.gz

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Quantitative Transcriptome Analysis of T cells stimulated with STING ligands

Project description:STING plays a key role in detecting cytosolic DNA and induces type I interferon responses for host defense against pathogens. Although T cells highly express STING, its physiological role remains unknown. In this study, we show that costimulation of T cells via TCR and STING ligand induce type I IFN responses like innate immune cells.

2017-10-10 | GSE104725 | GEO

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.

2022-08-10 | GSE199343 | GEO

Intrinsic self-DNA triggers inflammatory disease dependent on STING (I)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart

2014-07-09 | E-GEOD-59217 | biostudies-arrayexpress

Single-cell gene expression profiles of mouse macrophages stimulated with immune ligands.

Project description:Single-cell gene expression profiles of mouse macrophages stimulated with immune ligands.

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Single-cell gene expression profiles of mouse macrophages stimulated with immune ligands

Project description:Single-cell gene expression profiles of mouse macrophages stimulated with immune ligands

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Gene expression profiling of human telomerase fibroblasts stimulated with dsDNA90

Project description:Gene expression analysis of dsDNA90 stimulated human telomerase fibroblasts (hTERT-BJ1) after STING siRNA treatment. Genes whose expression that are affected by cytosolic DNA in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated. hTERT-BJ1 cells were transfected with non-specific or STING siRNA for 72 hours followed by dsDNA90 stimulation for 3 hours. Total RNA was extracted for array analysis.

2013-01-15 | E-GEOD-43480 | biostudies-arrayexpress

RNA-Sequencing of STING competent and STING-KO cells after transfection with dacA (Listeria monocytogenes)

Project description:HEK-Blue™ ISG Cells and HEK-Blue™ ISG-KO-STING Cells (Invivogen) were transfected with dacA (Listeria monocytogenes) for 12 and 24 hours. Through this approach, we described the STING-dependent and STING-independent transcriptional response to dacA. Our analysis reveals a STING-dependent enrichment of interferon stimulated genes beginning 12 hours post-transfection, and a STING-independent enrichment of genes associated with protein translation and oxidative phosphorylation.

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Dendritic cell stimulation: 5 ligands, 9 time points

Project description:mouse primary BMDCs were stimulated with tlr ligands and gene expression changes were profiled on Affymetrix arrays BMDC were stimulated with 5 tlr ligands (LPS, pIC ,PAM, CpG, GRD) across 9 time points (.5, 1, 2, 4, 6, 8, 12, 16, 24 hours). Unstimulated cells were used as controls.

2010-06-21 | E-GEOD-17721 | biostudies-arrayexpress

Intrinsic self-DNA triggers inflammatory disease dependent on STING (II)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), Trex1 deficient MEFs (TKO) or STING and Trex1 double deficient MEFs (STKO) transfected with or without double strand DNA 90 (ISD) and examined cytokine production by these cells.

2014-07-09 | E-GEOD-59218 | biostudies-arrayexpress

Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.

2014-05-31 | E-GEOD-57603 | biostudies-arrayexpress

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