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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Dependency of ISG expression on IFNAR1 and Tyk2

ABSTRACT: We analyze the expression profile of ISGs in the context of IFNAR1-KO primary murine B cells and macrophages. These analses were used to define ISG gene sets that are under tonic control. Furthermore, these analyses enabled the definition of ISGs that are dependent on Tyk2 signaling. Male C57BL/6 IFNAR1-KO mice were injected subcutaneously with 10,000U IFNa for 2hrs. Splenic B cells and peritoneal macrophages were sorted by FACS directly into TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

ORGANISM(S): Mus musculus

SUBMITTER: CBDM Lab

PROVIDER: E-GEOD-75203 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dependency of ISG expression on IFNAR1 and Tyk2

Project description:We analyze the expression profile of ISGs in the context of IFNAR1-KO primary murine B cells and macrophages. These analses were used to define ISG gene sets that are under tonic control. Furthermore, these analyses enabled the definition of ISGs that are dependent on Tyk2 signaling.

2015-11-20 | GSE75203 | GEO

Herpes simplex encephalitis in a patient with a new form of inherited IFNAR1 deficiency

Project description:Inborn errors of TLR3-dependent IFN-α/β- and -λ-mediated immunity in the central nervous system (CNS) can underlie herpes simplex virus 1 (HSV-1) encephalitis (HSE). The respective contributions of IFN-α/β- and -λ are unknown. We report a child homozygous for a genomic deletion of the entire coding sequence and part of the 3’UTR of the last exon of IFNAR1, who died from HSE at the age of two years. An older cousin died following vaccination against measles, mumps and rubella at 12 months of age, and another 17-year-old cousin homozygous for the same variant has had other viral illnesses. The encoded IFNAR1 protein is expressed on the cell surface but is truncated and cannot interact with the tyrosine kinase TYK2. The patient’s fibroblasts and EBV-B cells did not respond to IFN-α2b or IFN-β, in terms of STAT1, STAT2 and STAT3 phosphorylation, or the induction of IFN-stimulated genes (ISGs). Transcriptome analysis revealed a complete abolition of genome-wide ISG induction in response to IFN-α2b in IFNAR1-deficient fibroblasts from the patient. These fibroblasts were susceptible to viruses, including HSV-1, even in the presence of exogenous IFN-α2b or IFN-β. HSE is therefore a consequence of inherited complete IFNAR1 deficiency. This experiment of Nature indicates that IFN-α/β are essential for anti-HSV-1 immunity in the CNS.

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Project description:ISG induction in IFNAR2 mutant, IFNAR1 KO and wild type THP1

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Kinetics of IFNa response

Project description:We describe finely resolved kinetics of the transcriptional response to IFNa in B cells in vivo. Temporal changes in expression of the most robustly induced ISGs were analyzed across 23 (15min - 15hrs) timepoints. Most ISGs reach peak induction at approximately 2hrs and generally in a synchronus manner. These analses provide insight into the regulatory network structure of IFN responses. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa according to time course profile. Splenic B cells were sorted by FACS directly into TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

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Cell specific response to IFNa

Project description:We report cell specific responses to IFNa in 11 different peripheral immunocyte populations in the mouse. These cells represent the core ImmGen immunocyte lineage panel. Profiles from these were used to analyze cell specific responses to IFNa. In general a core set of ISG transcripts are induced in all cells. Smaller sets of ISGs were induced in a cell specific manner. In particular, splenic granulocytes and dendritic cells show restriced indcution of sets of ISGs. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa according to time course profile. Splenocytes/Peritoneal lavage suspensions were stained in multicolor antibody panels that were used to distinguish 11 different immunocyte populations (Immgen 11 cell set). These cells were sorted by FACS directly into TriZo and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

2015-11-20 | E-GEOD-75202 | biostudies-arrayexpress

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptome profile in IEC 4.1-WT and IEC4.1-Ifnar1-/- KO cells (C12 KO) in response to Cryptosporidium parvum

Project description:This study aims to measure the impact of Ifnar1-/- knockdown (KO) on the transcriptome profile in cultured IEC 4.1 cell in response to C. parvum infection. IEC4.1-WT cells and IEC4.1-Ifnar1-/- cells (stably CRISPR/Cas9 knockout; C12 KO cells) were exposed to C. parvum infection. Cells treated with a scrambled non-specific siRNA were used as the control. Total RNA was collected for the genome-wide analysis.

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Transcriptome analysis of peripheral blood from Lyn-deficient mouse SLE model lacking Ifnar1 or Irf5

Project description:To clarify the role of interferon regulatory factor 5 (IRF5) other than inducing type I interferons (IFNs) in the pathogenesis of systemic lupus erythematosus (SLE), we performed transcriptome analysis of peripheral blood from Lyn-deficient mice with concomitant Ifnar1 or Irf5 deficiency. The results of gene set enrichment analysis (GSEA) suggest that IRF5 is involved in the induction of not only IFN-inducible genes (ISGs) but also oxidative phosphorylation (OXPHOS)-related genes in the SLE pathogenesis.

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IFNAR1 Signaling in NK Cells Promotes Persistent Virus Infection

Project description:Inhibition of IFN-I signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here we report that genetic ablation of IFNAR1 specifically in NK cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells, resulting in hastened virus clearance comparable to IFNAR1 blockade by an IFNAR1 neutralizing antibody. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell maturation, function, and killing of antigenspecific CD4 and CD8 T cells. Therefore, Inhibition of IFN I signaling in NK cells enhances CD4 and CD8 T cell responses, elevates humoral immune response, and thereby facilitates the control of persistent virus infection.

2021-03-30 | GSE147330 | GEO

Transcriptome analysis reveals a major impact of Tyk2 on the expression of interferon responsive and metabolic genes

Project description:Peritoneal macrophages of Tyk2-/- and wildtype (wt) mice were compared before and after six hours of LPS treatment. Interferon responsive genes are lower expressed in Tyk2-/- macrophages at the basal level, metabolic genes higher before, but even more after LPS treatment. cDNA from macrophages from three replicates of three Tyk2-/- and three wt mice before and after six hours of LPS treatment, respectively, was hybridized to a microarray and analyzed.

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