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Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

ABSTRACT: Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

PROVIDER: PRJNA113777 | ENA |

REPOSITORIES: ENA

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Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

Project description:This SuperSeries is composed of the following subset Series: GSE11926: Transcriptional profiles of Ad-F3 and Ad-F7 transduced macrophages. GSE12002: Transcriptional profiles of Ad-F7 transduced macrophages in the presence of neutralizing antibody for the type I interferon receptor (IFNAR2) or control isotype (IgG). Refer to individual Series

2008-11-29 | E-GEOD-12120 | biostudies-arrayexpress

Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.

Project description:The immunoregulatory transcriptional modulators - IFN-regulatory factor (IRF)-3 and IRF-7 - possess similar structural features but distinct gene-regulatory potentials. For example, adenovirus-mediated transduction of the constitutively active form of IRF-3 triggered cell death in primary human MPhi, whereas expression of active IRF-7 induced a strong anti-tumoral activity in vitro. To further characterize target genes involved in these distinct cellular responses, transcriptional profiles of active IRF-3- or IRF-7-transduced primary human MPhi were compared and used to direct further mechanistic studies. The pro-apoptotic BH3-only protein Noxa was identified as a primary IRF-3 target gene and an essential regulator of IRF-3, dsRNA and vesicular stomatitis virus-induced cell death. The critical role of IRF-7 and type I IFN production in increasing the immunostimulatory capacity of MPhi was also evaluated; IRF-7 increased the expression of a broad range of IFN-stimulated genes including immunomodulatory cytokines and genes involved in antigen processing and presentation. Furthermore, active IRF-7 augmented the cross-presentation capacity and tumoricidal activity of MPhi and led to an anti-tumor response against the B16 melanoma model in vivo. Altogether, these data further highlight the respective functions of IRF-3 and IRF-7 to program apoptotic, immune and anti-tumor responses.

| S-EPMC2773157 | biostudies-literature

Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

Project description:This SuperSeries is composed of the SubSeries listed below.

2008-11-30 | GSE12120 | GEO

Expression profiles of IRF-1 silenced ovarian cancer cell lines

Project description:Ovarian cancer cells treated with CDDP showed up-regulation of IRF-1 and IRF-7. The expression of putative IRF-1 target genes was modulated. CDDP triggered nuclear translocation of IRF-1 and IRF-1 silencing re-orchestrated the expression profiles of CDDP treated cells.

2013-12-31 | GSE38551 | GEO

Expression profiles of IRF-1 silenced ovarian cancer cell lines

2013-12-31 | E-GEOD-38551 | biostudies-arrayexpress

Metabolic re-programming by MALAT1 depletion in prostate cancer

Project description:Metabolic re-programming by MALAT1 depletion in prostate cancer

| PRJNA615392 | ENA

Cell origin dictates programming of resident versus recruited macrophages during acute lung injury

Project description:The primary objective of this study was to compare global differences in transcriptional programming of resident and recruited alveolar macrophages in a time-limited murine model of lung inflammation. We first performed RNA sequencing of the resident and recruited alveolar macrophages from initiation through resolution of LPS-induced lung inflammation in the mouse. Our results indicate that despite existing in a shared environment, cell origin is the major determinant of programming of resident and recruited AMs during an acute inflammatory response. Major areas of difference include cell proliferation, inflammatory cytokine production and metabolism.

2017-09-19 | GSE94749 | GEO

Transcription profiling of mouse primary macrophages treated with the chemotherapeutic agent, 5,6-dimethylxanthenone-4-acetic acid,

Project description:Vascular disrupting agents (VDA) represent a novel approach to the treatment of cancer, resulting in collapse of tumor vasculature and tumor death. 5,6-Dimethylxanthenone-4-acetic acid (DMXAA) is a VDA currently in advanced Phase II clinical trials, yet its precise mechanism of action is unknown despite extensive preclinical and clinical investigations. The data presented herein demonstrate that DMXAA is a novel and specific activator of the TBK1-IRF-3 signaling pathway. DMXAA treatment of primary murine macrophages resulted in robust IRF-3 activation, a ~750-fold increase in IFN-beta mRNA and, in contrast to the potent Toll-like receptor 4 (TLR4) agonist, lipopolysaccharide (LPS), signaling was independent of mitogen-activated protein kinase (MAPK) activation and elicited minimal NF-kappaB-dependent gene expression. DMXAA-induced signaling was critically dependent on the IRF-3 kinase, TBK1, and IRF-3, but MyD88-, TRIF-, IPS-1/MAVS-, and IKKbeta-independent, thus excluding all known TLRs and cytosolic helicase receptors. DMXAA pretreatment of murine macrophages induced a state of tolerance to LPS and vice versa. In contrast to LPS stimulation, DMXAA-induced IRF-3 dimerization and IFN-beta expression were inhibited by salicylic acid (SA). These findings detail a novel pathway for TBK-1-mediated IRF-3 activation and provide new insights into the mechanism of this new class of chemotherapeutic drugs. Experiment Overall Design: Microarray analysis was carried out using AffymetrixÂ® mouse array 430A_2 exposed to total RNA prepared from C57BL/6J or IFN-beta-/- macrophages that had been treated with medium alone or DMXAA for 3 h. Fold-induction was calculated using AffymetrixÂ® GeneChipÂ® Operating Software. A >3-fold increase or decrease between inducible and basal mRNA levels was set as the criteria for inclusion of a gene as modulated.

2008-06-15 | E-GEOD-7194 | biostudies-arrayexpress

Inhibition of Hepatocellular Carcinoma Progression by Forced Metabolic Re-Programming

Project description:Inhibition of Hepatocellular Carcinoma Progression by Forced Metabolic Re-Programming

| PRJNA478592 | ENA

The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function

Project description:The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function

| PRJNA1095533 | ENA

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