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Genome-wide RNA-seq transcriptional analysis of splenocyte responses to Dengue virus infection in WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) mice.

ABSTRACT: Genome-wide RNA-seq transcriptional analysis of splenocyte responses to Dengue virus infection in WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) mice.

PROVIDER: PRJNA411999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6068850.fastq.gz	Fastqsanger.gz
	SRR6068860.fastq.gz	Fastqsanger.gz
	SRR6068870.fastq.gz	Fastqsanger.gz
	SRR6068851.fastq.gz	Fastqsanger.gz
	SRR6068861.fastq.gz	Fastqsanger.gz

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Genome-wide RNA-seq transcriptional analysis of splenocyte responses to Dengue virus infection in WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) mice.

Project description:Interferon-regulatory factors (IRFs) are a family of transcription factors (TFs) that play critical roles in translating viral recognition into antiviral responses, including type I IFN production. Dengue virus (DENV) and other clinically important flaviviruses are controlled by functional type I interferon (IFN) responses. Using an experimental model of DENV infection that recapitulates key aspects of the human disease in mice, we demonstrate that while mice lacking the type I IFN receptor (Ifnar1-/-) succumb to DENV infection, mice that are deficient in IRF-3, IRF-5, and IRF-7 – the three transcription factors thought to regulate type I IFN production – survive DENV challenge. Genome-wide RNA-seq analysis of WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) splenocytes identified minimal type I IFN production but a robust type II IFN (IFN-γ) response in DKO and TKO mice later shown to be dependent on IRF-1. These results reveal a key role for IRF-1 in antiviral defense by activating both type I and II IFN responses during DENV infection.

2017-11-07 | GSE104189 | GEO

Irf3 phenotyping

Project description:The interferon regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to influenza A virus infections in Irf3-/-, Irf7-/- and Irf3-/-Irf7-/- knock-out mice.

2016-11-02 | GSE77600 | GEO

DNA-binding of IRF3, IRF5 and IRF7 transcription factors

Project description:DNA-binding of IRF3, IRF5 and IRF7 transcription factors

| PRJNA429664 | ENA

Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:To investigate the role of the IRF family in the regulation of interferon stimulated genes, we conducted CRISPR/Cas9 mediated genome editing of Irf3, Irf7 or Irf9 in sgScd2 Th1 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of control, sgScd2, sgScd2/sgIrf3, sgScd2/sgIrf7 or sgScd2/sgIrf9 Th1 cells.

2022-08-03 | GSE200636 | GEO

IRF3-mediated pathogenicity in a murine model of human hepatitis A

Project description:Hepatitis A virus (HAV), an hepatotropic picornavirus, is a common cause of acute hepatitis in human populations. Although responsible for considerable morbidity and mortality, the mechanisms underlying HAV-mediated liver injury are poorly understood. Ifnar1-/- mice are susceptible to HAV and when infected recapitulate cardinal features of hepatitis A in humans, including serum ALT elevation, hepatocellular apoptosis, and intrahepatic inflammatory cell infiltrates. In contrast, Mavs-/- mice, while equally permissive for infection, experience no liver injury. Previous studies indicate that HAV pathogenesis in Ifnar1-/- mice is dependent upon MAVS-IRF3 signaling, but leave unresolved the role of IRF3-mediated transcription versus non-transcriptional pro-apoptotic activity of activated IRF3 in HAV-induced liver disease. Here, we compared the intrahepatic transcriptomes of HAV-infected naïve Mavs-/- and Ifnar1-/- mice using high throughput RNA sequencing, and characterized IRF3-mediated transcriptional responses associated with hepatocyte apoptosis and liver inflammation.

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mouse splenocyte

Project description:mouse splenocyte Raw sequence reads

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Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

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Silencing of Irf7 pathways in breast cancer cells promotes bone metastasis through immune escape mechanisms

Project description:Breast cancer metastasis to bone is a critical determinant of long-term survival after treatment of primary tumors. We used a mouse model of spontaneous bone metastasis to determine new molecular mechanisms. Differential transcriptome comparisons of primary and metastatic tumor cells revealed that a substantial set of genes suppressed in bone metastases were highly enriched for promoter elements for the type I interferon (IFN) regulatory factor, Irf7, itself suppressed in mouse and human metastases. The critical function of the Irf7 pathway was demonstrated by restoration of exogenous Irf7 or systemic interferon administration, which significantly reduced bone metastases and prolonged metastasis free survival. Using mice deficient in the type I receptor (Ifnar1-/-) or mature B, T and NK cell responses (NOD Scid IL-2rÎ³-/- mice) we demonstrated that Irf7-driven suppression of metastasis was reliant on IFN signaling to host immune cells. Metastasis suppression correlated with decreased accumulation of myeloid-derived suppressor cells and increased CD4++, CD8 T cells and NK cells in the peripheral blood and was reversed by depletion of CD8+ cells and NK cells. Clinical importance of our findings was demonstrated as increased primary tumor Irf7 expression predicted prolonged bone and lung metastasis-free survival. Thus we report for the first time, a novel innate immune pathway, intrinsic to breast cancer cells, whose suppression in turn restricts systemic immunosurveillance to enable metastasis. This pathway may constitute a novel therapeutic target for restricting breast cancer metastases. Comparison of basal gene expression in breast cancer 4T1.2 cell line stably transfected using the pMSCV retroviral expression vector system with IRF7 or the base vector. Three independent experiments were performed comparing the IRF7 expressing cells to the base vector cells

2012-07-17 | E-GEOD-37828 | biostudies-arrayexpress

ChIP-seq for IRF7

Project description:We performed ChiP-Seq for IRF7 in GM-CSF induced bone-marrow cells. IRF7 ChIP-Seq in myeloid cells

2014-12-03 | E-GEOD-62697 | biostudies-arrayexpress

Gene expression in IRF3-/- peritoneal macrophage infected with VSV

Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.

2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress

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