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Defining precision probes which differentiate between the activity of type I and type II interferons.

ABSTRACT: To define probes which differentiate between the activity of type I or type II IFN, a human submandibular gland (HSG) cell line was cultured for 48 hours in the absence or presence of IFNa or IFNg. Gene expression was assayed at 4, 12, 24 or 48 hours and was compared to gene expression in untreated cells at each time point to define genes which are induced by type I or type II IFN.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41291 | GEO | 2012/10/08

SECONDARY ACCESSION(S): PRJNA176459

REPOSITORIES: GEO

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Defining precision probes which differentiate between the activity of type I and type II interferons.

Project description:To define probes which differentiate between the activity of type I or type II IFN, a human submandibular gland (HSG) cell line was cultured for 48 hours in the absence or presence of IFNa or IFNg. Gene expression was assayed at 4, 12, 24 or 48 hours and was compared to gene expression in untreated cells at each time point to define genes which are induced by type I or type II IFN. HSG cells were cultured for 2 days in the absence or presence of IFNa [1000U/ml] or IFNg [50ng/ml], and total RNA was isolated at 4, 12, 24, and 48 hours of culture. Details are in the Analytical Methods section of the manuscript: John C. Hall, Livia Casciola-Rosen, Alan E. Berger, Efstathia Kapsogeorgou, Chris Cheadle, Athanasios G. Tzioufas, Alan N. Baer, Antony Rosen,Precise probes of type II interferon activity define the origin of interferon signatures in target tissues in rheumatic diseases accepted for publication in PNAS (this GEO dataset will be released immediately upon electronic publication).

2012-10-08 | E-GEOD-41291 | biostudies-arrayexpress

Type I and II Interferon-Stimulated Genes in Murine Primary Bone Marrow Macrophages

2012-02-15 | GSE35825 | GEO

FAT10 is phosphorylated by IKKβ to inhibit the antiviral type-I interferon response

Project description:Type-I interferon (IFN-I) secretion provides a rapid host defense against infection with RNA-viruses. Upon entry into the host cell, the viral RNA triggers the activation of both RIG-I and TLR3 signaling pathways, ultimately leading to the production of type-I interferons. Since an exaggerated IFNa/b response can cause severe tissue damage, these pathways are tightly regulated. One of the factors that keep the type 1 IFN response in check is the ubiquitin-like modifier FAT10. FAT10 is expressed upon synergistic stimulation with TNFα and IFNγ, and it targets covalently FAT10-linked substrate proteins for proteasomal degradation. However, the mechanism how FAT10 modulates IFN-I secretion remains to be fully elucidated. Here, we found that FAT10 is phosphorylated by Ikb kinase b (IKKβ) upon TNFα stimulation and during Influenza Virus infection on several serine and threonine residues. FAT10 phosphorylation increases the binding of FAT10 to the TRAF3-deubiquitylase OTUB1 and its FAT10-mediated activation. Consistently, FAT10 phosphorylation results in a low ubiquitylation state of TRAF3 which is unable to maintain IRF3 phosphorylation and downstream induction of type 1 IFNs. Taken together, we reveal a mechanism how the TNF-induced phosphorylation of FAT10 limits the production of tissue destructive IFN-I in inflammation.

2023-11-07 | PXD028918 | Pride

IKK-epsilon regulates the balance between the type I and type II interferon responses

Project description:Virus infection induces the production of type I and type II interferons (IFN-I and IFN-II), cytokines that mediate the antiviral response. IFN-I (IFN-a and -b) induces the assembly of ISGF3 (interferon-stimulated gene factor 3), a multimeric transcriptional activation complex comprised of STAT1, STAT2 and IRF9. IFN-II (IFN-g) induces the homodimerization of STAT1 to form the GAF (gamma-activated factor) complex. ISGF3 and GAF bind specifically to distinct regulatory DNA sequences located upstream of IFN-I and II inducible genes, respectively, and activate the expression of distinct set of antiviral genes. The balance between the type I and type II IFN pathways plays a critical role in orchestrating the innate and adaptive immune systems. Here, we show that the phosphorylation of STAT1 by IKKε (IkB-related kinase epsilon) inhibits STAT1 homodimerization, and thus GAF formation, but does not disrupt ISGF3 formation. Therefore, virus and/or IFN-I activation of IKKε suppresses GAF-dependent transcription and promotes ISGF3-dependent transcription. In the absence of IKKε, GAF-dependent transcription is enhanced at the expense of ISGF3-mediated transcription, rendering cells less resistant to infection. We conclude that IKKε plays a critical role in regulating the balance between the IFN-I and IFN-II signaling pathways.

2011-12-01 | GSE33913 | GEO

Type I and II Interferon-Stimulated Genes in Murine Primary Bone Marrow Macrophages

Project description:We used microarrays to compare interferon-alpha (IFNa)- and interferon-gamma (IFNg)-stimulated genes under an equivalent biological input. The goal was to compare IFNa- and IFNg-stimulated genes, as well as to identify common and distinct sets of type I and II ISGs. Bone marrow macrophages derived from mouse bone marrow in M-CSF for 7 days. The cells were stimulated with 62U/mL IFNa and 1U/mL of IFNg for 2.5 hrs in culture. These concentrations induced equivalent STAT1 phosphorylation in BMMs.

2012-02-15 | E-GEOD-35825 | biostudies-arrayexpress

Transcription profiling of human BE(2)-C neuronal responses to type I IFN stimulation

Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation. Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks, incubated with universal type I IFN (IFNa-A/D) for 6 or 12 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.

2009-07-12 | E-GEOD-16450 | biostudies-arrayexpress

IKK-epsilon regulates the balance between the type I and type II interferon responses

2011-12-01 | E-GEOD-33913 | biostudies-arrayexpress

Genome-wide analysis of IFNa response in WT and STAT3KO MEFs

Project description:Analysis of gene expression profiles in MEF cell lines in the absence or presence of STAT3 following IFNa stimulation. This study is to unveil possible role of STAT3 during type I IFN-mediated gene induction and functions. Total RNA obtained from WT or STAT3KO MEFs stimulated without or with IFNa 1000 U/ml for 2 h.

2010-11-04 | E-GEOD-25044 | biostudies-arrayexpress

Transcription profiling of Type I interferon response of human blood monocytes primed with Type II interferon

Project description:Type I IFN-inducible gene expression in human blood monocytes primed with Type II IFN.

2007-08-04 | E-GEOD-1740 | biostudies-arrayexpress

Differential Gene Induction by Type I And Type II Interferons and Their Combination

Project description:Type I and type II interferons (IFNs) bind to different cell surface receptors but activate overlapping signal transduction pathways. We examined the effects of a type I IFN (IFN-acon1) and a type II iFN (IFN-g1b) on gene experession in A549 cells and demonstrate that there is a common set of genes modulated by both IFNs as well as a set of gene specifically regulated by each, reflecting the activation of different signaling pathways. In particualr, IFN-g induced many more genes of the signaling pathways, apoptosis, and cytokine interactions than did IFN-a. Even with genes induced by both IFNs there were distinctive quantitativive differences in expression. IFN-g1b plays a major role in the induction and regulation of the complement pathway. Previous work has shown a synergistic antivral and antiproliferative effect of type I and type II IFNs in cell culture and in the treament of tumors in mice. We demonstrate that a majority of genes showed and additive effect of IFN-acon1 and IFN-g1b, but a subset of gene is synergistically induced; these incluce ISG10, MX2, OAS2, and other genes known to be involved in the antiviral response, TRAIL (TNFSF10) and caspases involved in apoptosis and chemokine genes RANTES, CXCL10, and CXCL11. Greater than additive transcription of some of these genes in the presence of both IFNs was confirmed by real-time kinetic RT-PCR. Elevated induction of many of these genes may be sufficient to explain the synergistic antiviral and antitumor effects of this combination of IFNS in vivo. Keywords: comparison of 2 treatments, combination, and untreated at two time points

2006-08-15 | GSE5542 | GEO

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