Comparative analysis of gene expression upon IFNα stimulation in hepatocyte-like cells [IFN]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1216564 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32151283.fastq.gz | Fastqsanger.gz | |||
| SRR32151284.fastq.gz | Fastqsanger.gz | |||
| SRR32151285.fastq.gz | Fastqsanger.gz | |||
| SRR32151286.fastq.gz | Fastqsanger.gz | |||
| SRR32151287.fastq.gz | Fastqsanger.gz |
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Project description:Patients chronically co-infected by Hepatitis B Virus (HBV) and Hepatitis D Virus (HDV) suffer from the most aggressive form of viral hepatitis leading to severe liver disease such as cirrhosis, hepatocellular carcinoma and liver decompensation. Treatments options are very limited with only two drugs used in clinic (IFN-α and Bulevertide) that rarely allow viral clearance. The molecular mechanisms leading to inhibition of HDV by IFN-α (in patients but also in vitro) are not known and mechanisms behind treatment failures in patients also remain elusive. Here we aimed at the identification of interferon stimulated genes (ISGs) that can specifically inhibit intracellular HDV replication. IFN-α was able to inhibit HDV in both co-infected differentiated HuH7.5-NTCP- and HepaRG cells (dHuH7.5-NTCP and dHepaRG, respectively). We hypothesized that ISGs responsible for the antiviral effect of HDV should be upregulated in both dHepaRG and dHuH7.5-NTCP cells upon treatment with IFN-α. To identify these ISGs, dHuh7.5-NTCP and dHepaRG cells were stimulated with IFN-α for 8h, total RNAs were extracted and gene expression was analyzed by RNAseq.
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Project description:Interferon-α (IFNα) plays a key role in innate immunity by inducing interferon-stimulated genes (ISGs). Beyond protein-coding ISGs, non-coding RNAs such as microRNAs are also modulated by IFNα. Here, we profiled differentially expressed microRNAs in HepG2 cells following IFNα stimulation, providing new insights into interferon signaling and antiviral regulation.
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Project description:IFN-γ stimulation induces immunosuppression in CRC
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Project description:To investigate differentially expressed genes (DEGs) upon challenge with infectious salmon anemia virus (ISAV) or infectious pancreatic necrosis virus (IPNV) after IFNα treatment, in comparison to untreated cells. To examine the differentially expressed genes (DEGs) in knock-out (KO) cells with specific IFN receptors knockout, following IFNα treatment and infection with ISAV or IPNV. The expression profiles of these KO cells were compared with non-KO cells also treated with IFNα and infected with ISAV or IPNV.
2023-12-01 | E-MTAB-13068 | biostudies-arrayexpress
Project description:Type I interferon is naturally produced in response to pathogens to generate an anti-viral state within the cell. There are 13 naturally occurring genetic isoforms of IFN alpha (IFNα) in humans that result in 12 IFNα subtypes (IFNα1 and α13 are identical but are coded by different genes). They all bind the same ubiquitously expressed receptor, interferon alpha receptor (IFNAR), but have been shown to differ in their biological and anti-viral activities (reviewed in Gibbert et al, Br J Pharmacol 2013). We investigated the ability of natural and recombinant IFNα to regulate mRNA expression. Here we present a dataset comprising whole genome microarray data from primary human monocyte-derived macrophages following treatment with different preparations of IFNα. These data are suitable for determination of IFN-stimulated genes, and additionally allow differential analysis of gene induction in response to natural versus recombinant IFNα. For example, this comparison may be useful in identifying cellular anti-viral effector proteins involved in viral restriction, thus potentially providing novel therapeutic approaches without the historical negative outcomes of IFNα therapy.
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Project description:The study of the interferon (IFN) α-induced cell transcriptome has shown altered expression of several long non-coding RNAs (lncRNAs). ISR8 / IRF1-AS1 (IFN stimulated RNA 8), located close to IFN regulatory factor 1 (IRF1) coding gene, transcribes a lncRNA induced at early times after IFNα treatment or IRF1 or NF-κB activation. Depletion or overexpression of ISR8 RNA does not lead to detected deregulation of the IFN response. Surprisingly, disruption of ISR8 locus with CRISPR-Cas9 genome editing results in cells that fail to induce several key ISGs and pro-inflammatory cytokines after a trigger with IFNα or overexpression of IRF1 or the NF-κB subunit RELA. This suggests that the ISR8 locus may play a relevant role in IFNα and NF-κB pathways. Interestingly, IFNα, IRFs and NF-κB-responding luciferase reporters are normally induced in ISR8-disrupted cells when expressed from a plasmid but not when integrated into the genome. Therefore, IFNα and NF-κB pathways are functional to induce the expression of exogenous episomic transcripts but fail to activate transcription from genomic promoters. Transcription from these promoters is not restored with silencing inhibitors, by decreasing the levels of several negative regulators or by overexpression of inducers. Transcriptome analyses indicate that ISR8-disrupted cells have a drastic increase in the levels of negative regulators such as XIST and Zinc finger proteins. Our results agree with ISR8 loci being an enhancer region that is fundamental for proper antiviral and proinflammatory responses. These results are relevant because several SNPs located in the ISR8 region are associated with chronic inflammatory and autoimmune diseases including Crohn’s disease, inflammatory bowel disease, ulcerative colitis or asthma.
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Project description:This SuperSeries is composed of the following subset Series: GSE17299: Direct effects of IFNα on human CD8 T cells_without any other concomitant signals GSE17301: The effect of IFNα on human CD8 T cells_with other concomitant signals Refer to individual Series
2010-07-23 | E-GEOD-17302 | biostudies-arrayexpress
Project description:IFNα-mediated gene expression pattern. Direct effects of IFNα on human CD8 T cells without any other concomitant signal. This analysis examined the direct effects of IFNa on human CD8 T cells without any other concomitant signal. Total human CD8 T cells were magnetically sorted from peripheral blood by negative selection. In order to minimize the presence of antigen-experienced cells, total human CD8 T cells were depleted of CD45RO+ cells by labelling with anti-CD45RO magnetic bead. In both steps of cellular sorting, negative selection were preferred to positive selection to avoid direct labelling of CD8 T cell surface molecules could interfere with downstream IFNa-mediated signalling. Magnetically sorted untouched human CD8+CD45R0- T cells from three different donors were unstimulated or stimulated with IFNa2b or IFNa5 and cells were harvested 7 hours later. mRNAs from the 3 subjects were pooled and analyzed using Affymetrix human HG-U133A 2.0 array gene chips Fold-change ≥ 2 criterion was used to identify genes which expression differed between treatment and control (unstimulated cells). Keywords: Gene expression pattern analysis Magnetically sorted untouched CD8+CD45R0-T cells mRNA pooled sample from three different donors unstimulated or stimulated with IFN alfa 2b or IFN alfa 5 for 7 hours.
2010-07-23 | E-GEOD-17299 | biostudies-arrayexpress