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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

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

Transcription profiling of human A549 cell line treated with type I and II interferons vs. controls

2007-11-02 | E-GEOD-5542 | biostudies-arrayexpress

Influence of type I Interferons on function of splenic conventional dendritic cells.

2009-07-07 | GSE12392 | GEO

Delayed induction of type I and III interferons enhances nasal epithelial permissiveness to SARS-CoV-2

Project description:We provide the first comprehensive analysis of nasal cell responses to SARS-COV-2 using single cell transcriptomics and proteomics. The immune response to SARS-CoV-2 is dominated by a delayed type I and III IFN response, which is too slow to contain viral replication. Cells transitioning from secretory to ciliated states are highly permissive to SARS-CoV-2, whereas goblet cells are relatively resistant. Cell-type differences in the production and response to IFN-I/III correlate with permissiveness. Pre-treatment with recombinant IFNs potently restricts SARS-CoV-2. Nasal delivery of recombinant IFNs is a promising prophylactic strategy for SARS-CoV-2

2021-05-25 | PXD022523 | Pride

Modulation of T cell responses by type I interferons

Project description:Type I interferons (IFNs) play a key role in linking the innate and adaptive immune responses. IFNs can have both positive and negative effects on the development of memory CD8+ T cells, but their contribution to the priming of naÃ¯ve T cells is unclear. Using OT-I TCR transgenic T cells, we show strong effects on TCR-induced functional response when sensitized by IFN-Î² prior to their stimulation with cognate antigen. These effects are only seen in the absence of co-stimulation and at suboptimal TCR stimulation conditions. Pre-stimulation of naÃ¯ve T cells inhibits certain TCR-mediated functions like cell proliferation and the induction of genes such as IFN-Î³ and IL-2. However, type I IFN does not influence the induction of other TCR-induced functions like the expression of the T cell activation marker CD25 and a number of other genes. IFN-mediated impairment of proliferation is due to the lack of IL-2 induction since it can be compensated by exogenous IL-2. Further analysis reveals an IFN-mediated inhibition of Ca2+ flux and ERK phosphorylation. In vivo studies confirm that pre-stimulation with IFNs inhibits early T cell responses, whereas long-term responses are positively affected. Our results reveal that IFN exerts negative effects on naÃ¯ve T cells in a timely defined range under sub-optimal TCR stimulation conditions. These results highlight the importance of timing of immune-regulatory events and reveal a novel role for type I IFNs by shaping the immune response, such that T cells are not able to react until optimal stimulation is provided. 8 Arrays, untreated cells as references, IFNb treatment and/or TCR stimulation at various lengths of time

2015-12-31 | E-GEOD-41381 | biostudies-arrayexpress

Transcriptomic Profiling of Collaborative Cross Founder Mouse Embryonic Fibroblasts stimulated with Type I, II and III Interferons

Project description:Collaborative Cross (CC) mouse embryonic fiborolasts (MEF) cells obtained from the eight Founder animals [PWK/PhJ, NZO/HILtJ, NOD/ShiLtJ, WSB/EiJ, A/J, CAST, C57BL/6J, and 129/SvlmJ] were immortalized and the cell lines used to assess differences in transcriptional responses following treatment with type I, II and III recombinant mouse interferon. We collected transcriptome profiles for 8 CC MEF cell lines stimulated with either IFN-α or IFN-β for a total of 16 different biological conditions. Treated and mock samples were collected at 18 hr post-treatment and RNAs extracted and subjected to microarray.

2014-05-27 | E-GEOD-53057 | biostudies-arrayexpress

Influence of type I Interferons on function of splenic conventional dendritic cells.

Project description:Type I Interferons encompasses a large family of closely related cytokines comprising of at least 13 IFN-α isotypes and single IFN-β. Both IFN-α and IFN-β exert their activity through a common receptor IFNAR. Type I Interferons have broad regulatory effects and various subtypes of dendritic cells are influenced by this cytokines. In our study we asked question whether the low, constitutive levels of type I Interferons produced under steady state conditions are important for proper function of splenic conventional dendritic cells. In this approach we sorted out two populations (CD8α+ and CD8α-) of splenic dendritic cells (DCs) from untreated WT, IFN-β-/- and IFNAR-/- C57Bl/6 mice. All mice were between 8-10 weeks old. Further we isolated RNA and performed microarray analysis. Each DCs population was repeated twice.

2009-07-07 | E-GEOD-12392 | biostudies-arrayexpress

Individual and combinatorial contribution of type I, II and III interferons in limiting SARS-CoV-2 replication, disease progression and age-related mortality [RN21061]

Project description:Using a mouse-adapted SARS-CoV-2 variant (SARS-CoV-2 MA), we found that endogenous type I and type III IFNs synergize to limit SARS-CoV-2 replication and to expedite virus clearance and that enhanced disease progression in aged mice depends on impaired type II IFN immunity

2022-09-19 | GSE190672 | GEO

Type I interferons govern Zika virus resistance of human macrophages and microglia

Project description:The role of the human type I interferon (IFN-I) system in restricting Zika virus (ZIKV) is uncertain. Here, genetic and pharmacological ablation of IFN-I signalling enhanced ZIKV replication and cytopathicity in macrophages and microglia, key cells in ZIKV transmission and pathogenesis. Thus, despite the extensive IFN-I countermeasures employed by ZIKV, IFN-I dictates the outcome of infection in macrophages. Therapeutic manipulation of the IFN-I system may bring clinical benefit in ZIKV.

2022-10-31 | GSE198542 | GEO

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