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Microarray data of human moDC treated with IFNβ and TNFα

ABSTRACT: Microarray data of human moDC treated with IFNβ and TNFα

PROVIDER: PRJNA554322 | ENA |

REPOSITORIES: ENA

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Microarray data of human moDC treated with IFNβ and TNFα

Project description:Human moDC were treated with IFNβ and TNFα or the combination of both for either 1 h or 2.5 h in triplicate and profiled by gene expression microarray

2020-11-30 | GSE134209 | GEO

Genome wide characterization of a STAT1-independent antiviral and immunoregulatory transcriptional program induced by IFNβ and TNFα reveals non-canonical STAT2 and IRF9 pathways

Project description:Interferon (IFN) β and Tumor Necrosis Factor (TNF) α are key players in immunity against pathogens as well as in the development of autoinflammatory and autoimmune diseases. Accordingly, their molecular pathways have attracted much interest as therapeutic targets. Compelling evidence has shown that the antiviral and inflammatory transcriptional response induced by IFNβ is reprogrammed by crosstalk with TNFα. IFNβ typically induces interferon-stimulated genes by the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway leading to activation of the canonical ISGF3 transcriptional complex, composed of STAT1, STAT2 and IRF9. The signaling pathways engaged downstream of the combination of IFNβ and TNFα remain elusive, but previous observations suggested the existence of a response independent of STAT1. Here, using genome-wide transcriptional analysis by RNASeq, we observed a broad antiviral and immunoregulatory response initiated in the absence of STAT1 upon IFNβ and TNFα costimulation. Additional stratification of this transcriptional response with respect to the role of STAT2 and IRF9 revealed that they mediate the expression of a wide spectrum of genes. While a subset of genes was regulated by the concerted action of STAT2 and IRF9, other gene sets were independently regulated by STAT2 or IRF9. Collectively, our data supports a model in which STAT2 and IRF9 act through non-canonical parallel pathways to regulate distinct pool of genes in response to IFNβ and TNFα. This study provides novel insights into the molecular pathways leading to antiviral and immunoregulatory gene expression in conditions where elevated levels of both IFNβ and TNFα are present.

2018-02-28 | GSE111195 | GEO

Control, TNFα and TNFα+JNK I treated GSCs

Project description:Control, TNFα and TNFα+JNK I treated GSCs

| PRJNA799754 | ENA

Gene expression profiling of C57BL/6J wildtype and IFNAR1 knockout mice following LPS and IFNβ stimulation

Project description:Type-I interferon signalling plays a critical role in immunity especially during viral infections. IFNAR1-deficent macrophages are highly resistant to Salmonella typhimurium (ST) infection and to the stimulation with LPS, poly I:C and TNFα. We have used microarray expression profiling on bone marrow derived macrophage cells as a discovery platform to identify genes that play a role in their resistance. Several genes were identified downregulated in IFNAR1-deficient macrophages compared to WT control sample. The Expression of identified genes will be quantified by qRT-PCR followed by knockdown of identified genes using si-RNA approach. The identified genes will help us to understand how IFNβ mediates susceptibility to bacterial infection in macrophages.

2024-08-15 | GSE134549 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of control, TNFα and TNFα+JNK I treated GSCs Transcriptomes

Project description:Among 830 TNFα-induced genes (at least 1.5 folds of upregulation in TNFα-treated TPC2-4 cells compared with control), the expression of 268 genes is significantly suppressed by JNKi treatment (TPC2-4 TNFα+JNKi/TPC2-4 TNFα, JNKi: JNK-IN-8, a kinase inhibitor specific for JNK (c-Jun N-terminal kinase) that inhibited phosphorylation of c-JUN)

2022-08-24 | GSE194220 | GEO

ATAC-seq comparatively analyse chromatin accessibility varition of control, TNFα and TNFα+JNK I treated GSCs

Project description:Among 3,673 TNFα-induced gain of accessibility (at least 2 folds of upregulation in TNFα-treated TPC2-4 cells compared with control), and most of the gained peaks were significantly suppressed by JNKi treatment (TPC2-4 TNFα+JNKi/TPC2-4 TNFα, JNKi: JNK-IN-8, a kinase inhibitor specific for JNK (c-Jun N-terminal kinase) that inhibited phosphorylation of c-JUN)

2022-08-24 | GSE194221 | GEO

Gene Expression Data in Human Monocyte-derived Dendritic Cell (MoDC) from Young and Aged Donors

Project description:Dendritic cells (DCs) are major antigen-presenting cells that play a key role in initiating and regulating innate and adaptive immune responses. DCs are critical mediators of tolerance and immunity. The functional properties of DCs changes with age. The purpose of this study was to define the age-associated molecular changes in DCs by gene array analysis using Affymatrix GeneChips. We identified up and down-regulated gene expression changes in DC from aged donors compared to young donors. Total 9 MoDC RNA samples from four young donors (20-27 years) and five aged donors (77-84 years) were analyzed using Affymetrix HG-U133A_2 Gene Arrays to compare differential gene expression changes in MoDC between aged and young groups

2014-05-28 | E-GEOD-58015 | biostudies-arrayexpress

Transcriptome analysis of IEC4.1 cells in response to TNFα stimulation.

Project description:Mouse intestinal epithelial cells (IEC4.1 cells) were stimulated with TNFα (10 ng/ml) for 4h. The Agilent SurePrint G3 Mouse Gene Expression Microarray (G4852A) was used for the analysis, which provides full coverage of genes and transcripts with the most up-to-date content, including mRNAs and lincRNAs (http://www.chem.agilent.com/store/en_US/Prod-G4852A/G4852A). IEC4.1 cells were grown to 80% confluence for four groups: the siRNA control (Group A, cells treated with a non-specific scrambied siRNA control), the TNFα -stimulated (Group B, cells treated with the siRNA control plus TNFα stimulation), lincRNA-Cox2 siRNA (Group C, cells treated with an siRNA to lincRNA-Cox2), and lincRNA-Cox2 siRNA/ TNFα stimulated (Group D, cells treated with the lincNRA-Cox2 siRNA plus TNFα stimulation). Cells were treated with the siRNAs for 24h, followed by additional culture for 4h in the presence or absence of TNFα (10 ng/ml). Total RNAs were prepared with the RNeasy Mini kit (Qiagen) according to the manufacturer’s instruction (Ambion).

2016-10-25 | E-MTAB-3904 | biostudies-arrayexpress

The effect of PRRSV on modulation of porcine monocyte-derived dendritic cell (MoDC)

Project description:To investigate the gene expression of MoDC after PRRSV stimulation and nucleocapsid protein transfection

2016-08-30 | GSE86182 | GEO

H3K4me3 HiChIP of immortalized human aortic endothelial cells treated with TNFα against untreated controls

Project description:TNFα is a potent cytokine to mediate inflammatory response by activation of the master transcription factor NF-kB. Endothelial cells are important participants in inflammatory responses in animals. NF-kB is a major mediator to activate endothelial cells by inducing multiple pro-inflammatory genes in response to TNFα. The process of transcriptional activation is dependent on the context of chromatin interactions/loops. However, the chromatin conformation in response to the cytokine challenge TNFα in human aortic endothelial cells has not been described. Our approach characterized chromatin interactions from active enhancers to promoters as well as active promoters to promoters on a genome-wide scale and highlighted important enhancer candidates for target genes.

2023-03-01 | E-MTAB-12213 | biostudies-arrayexpress

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