Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of healthy controls upon Interferon-beta stimulation

ABSTRACT: This experiment was carried out in the context of a pharmacogenetic study of long-term (4-year follow-up) response to Interferon-beta treatment in two cohorts of Italian Multiple Sclerosis patients, to identify genetic variants (SNPs) that may influence response to IFN-beta. We integrated results from meta-analysis of the two cohorts with gene expression profiling of IFNβ stimulated PBMCs from 20 healthy controls and eQTL analyses, to look at possible enrichment of IFN-beta induced genes with genes mapped by top-ranking meta-analyzed SNPs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71634 | GEO | 2015/08/03

SECONDARY ACCESSION(S): PRJNA291682

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of healthy controls upon Interferon-beta stimulation

Project description:This experiment was carried out in the context of a pharmacogenetic study of long-term (4-year follow-up) response to Interferon-beta treatment in two cohorts of Italian Multiple Sclerosis patients, to identify genetic variants (SNPs) that may influence response to IFN-beta. We integrated results from meta-analysis of the two cohorts with gene expression profiling of IFNβ stimulated PBMCs from 20 healthy controls and eQTL analyses, to look at possible enrichment of IFN-beta induced genes with genes mapped by top-ranking meta-analyzed SNPs. Total RNA obtained from isolated PBMC extracted from healthy subjects and in vitro stimulated or not with Interferon-β (100IU/mL) for 18h

2015-08-03 | E-GEOD-71634 | biostudies-arrayexpress

Expression data from 5 IFN type I-derived Dendritic Cells

Project description:Type I interferon (IFN) is a family of 15 cytokines (in human 13α, 1β,1ω) which exert several cellular functions through the binding to a common receptor. Despite the initial activation of the same Jak/Stat signalling pathway, the cellular response may be different depending on the type I IFN subtype. We investigated the activity of different type I IFN subtypes - IFNα1, α2, α8, α21, ω and β- on the differentiation of DC. Transcriptome analyses identified two distinct groups, the IFNα/ω-DC and the IFNβ-DC. 78 genes, 7 chemokines and expression levels of cell surface markers characteristic of DC distinguished IFNα-DC and IFNβ-DC. These differences are unlikely to impact the efficacy of T cell functional response since IFNα2-DC and IFNβ-DC were equipotent in inducing the proliferation and the polarization of allogenic naïve CD4 T cells into Th1 cells and in stimulating autologous memory CD4 or CD8 T cells. In contrast, IFNα2-DC were found to be more efficient than IFNβ-DC in the phagocytic uptake of dead cells. Human blood monocytes were differentiated in DC by using 5 differents IFN type I (IFNα2, α1, α8, α21 and β). After 3 days of differentiation RNA were extracted and analyzed by affymetrix microarray.

2012-09-20 | E-GEOD-40268 | biostudies-arrayexpress

Interferon inhibits a model RNA virus via a limited set of inducible effector genes [RNA-seq]

Project description:To investigate the transcripts induced by the cytokine interferon (IFN) β in U-2 OS cells, we treated U-2 OS cells with IFNβ 20U/mL for 6 and 24 hours and performed RNA-Seq to determine differentially expressed genes.

2023-05-26 | GSE233003 | GEO

Expression data from 5 IFN type I-derived Dendritic Cells

2012-09-20 | GSE40268 | GEO

Effect of chronic type I IFN exposure on the transcriptional, metabolic profiles of human monocyte-derived macrophages

Project description:The impact of chronic exposure to type I interferons (IFN)α2a,2b, and β, on macrophage metabolism, intimately linked to macrophage function, is not well understood. This study assesses the nuanced host responses induced by type I IFN cytokines, offering insights for potential therapeutic approaches in diseases associated with these cytokines. Employing a combination of transcriptional profiling and real-time functional analysis, we delineated the temporal evolution of metabolic reprogramming in response to chronic interferon exposure. Our results reveal distinct transcriptional metabolic profiles between macrophages chronically exposed to IFNα and IFNβ. IFNβ significantly diminishes the oxygen consumption rate and glycolytic proton extrusion rate in macrophages. Conversely, IFNα2b decreased parameters of mitochondrial fitness and induced a shift towards glutamine oxidation. Assessing the ability of macrophages to induce glycolysis in response to antigenic stimuli (LPS and iH37Rv), we found that chronic exposure to all IFN subtypes limited glycolytic induction. This study addresses a critical oversight in the literature, where individual roles of IFN subtypes are frequently amalgamated and lack distinction. These findings not only provide novel insights into the divergent effects of interferon α2a,α2b, and β on macrophage metabolism but also highlight their potential implications for developing targeted therapeutic strategies.

2024-07-29 | GSE268012 | GEO

ATF3 is a central regulator of interferon-beta and interferon-stimulated genes during the innate immune response

Project description:This study shows that in the absence of Atf3, primary mouse macrophages display significantly greater basal and PRR-inducible IFNβ expression. This regulation appears to be directly on the level of Ifnb1 transcription mediated by ATF3 binding proximal to the Ifnb1 promoter under basal condition. The ATF3 expression was demonstrated to be type I IFN-inducible in both human and mouse immune cells. A subset of 36 genes downstream of IFNAR signalling were modulated in an ATF3-dependent manner.The regulation of IFN responses by ATF3 had significant relevance on in vitro viral infection. Together these findings demonstrate that ATF3 is an important regulatory handbrake that limits the magnitude of IFN responses on multiple levels; basal Ifnb1 expression; PRR-inducible IFNβ; and the expression of specific ISGs. 12 samples

2015-09-07 | E-GEOD-61055 | biostudies-arrayexpress

IFNβ expression is restricted to a subpopulation of splenic pDCs exhibiting a specific immune modulatory transcriptome signature

Project description:Type I IFNs are critical in initiating protective antiviral immune responses and plasmacytoid DCs (pDCs) represent a major source of these cytokines. Here we show that only few pDCs are capable to produce IFNβ after virus infection or CpG stimulation. Utilizing IFNβ/YFP reporter mice, we identify these IFNβ-producing cells in the spleen as a CCR9+CD9- pDC subset exclusively localized within the T/B cell zones. IFNβ-producing pDCs exhibit a distinct transcriptome profile with higher expression of genes encoding cytokines and chemokines, facilitating T cell recruitment and activation. These distinctive characteristics of IFNβ-producing pDCs are independent of the type I IFN receptor mediated feedback loop. Furthermore, IFNβ-producing pDCs exhibit enhanced CCR7-dependent migratory properties in vitro and in a peritoneal inflammation model they effectively recruit T cells in vivo. We define “professional type I IFN-producing cells” as a distinct subset of pDCs specialized in coordinating cellular immune responses.

2015-05-27 | GSE68788 | GEO

Central Role of ULK1 in Type I Interferon Signaling

Project description:We provide evidence that the Unc-51-like kinase 1 (ULK1) is phosphorylated and activated during engagement of the Type I IFN receptor. Our studies demonstrate that the function of ULK1 controls expression of key interferon stimulated genes (ISGs) that mediate important biological functions, including anti-viral and antineoplastic responses. Total RNA was isolated from untreated and IFNβ-treated Ulk1/2+/+ and Ulk1/2-/- mouse embryonic fibroblasts (MEFs). Cells were treated for 6 hours with or without mouse IFNβ (2500 IU/ml).

2014-08-26 | E-GEOD-60778 | biostudies-arrayexpress

Expression data from rat INS-1E cells

Project description:Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476. Rat INS-1E cells were treated with cytokine cocktails (IL-1b, IFN-g and TNF-a) and/or BRD0476 for 6 or 12 hours. Total RNAs were isolated using the RNEasy kit from Qiagen.

2012-12-14 | E-GEOD-42897 | biostudies-arrayexpress

The transcriptome differences between IFN-I-elicited subsets of arginase 1-high and -low macrophages

Project description:Purpose: Using cells from the Arg1-YFP reporter mice, we discovered that only a part of macrophages from IFNβ-stimulated transitional monocytes showing Arg1-YFP expression. Therefore, we probed the overall differences between such IFN-I-elicited YFP+ and YFP- macrophages. Method: Bone marrow mononuclear cells from Arg1-YFP mice were treated with M-CSF± IFNβ for 64 h. The macrophages (F4/80+) in the control and IFN treatment group were further sorted by flow cytometry based on YFP intensities. The dominant YFP- population from the control cells (Con), as well as the YFP- (Treated1) and YFP+ (Treated2) subsets within IFNβ-treated cells were subjected to RNAseq analyses. Results: The most enriched biological functions for the up-regulated genes in the treated groups relate to immune activation, anti-viral responses and the IFN pathway. Most classical IFNβ downstream genes did not display differential expression between YFP- (Treated1) and YFP+ (Treated2). However, there are 84 genes displaying “Treated2 above Treated1” and 98 genes showing “Treated1 above Treated2” patterns. Conclusions: Our result show that IFN-I-elicited YFP+ and YFP- monocyte-derived macrophages tend to be M2- and M1-skewed, respectively.

2021-06-08 | GSE161428 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data