Gene expression profiling of C57BL/6J wildtype and IFNAR1 knockout mice following LPS and IFNβ stimulation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA555572 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Interferon-alpha/beta-receptor (IFNAR) signal defects were recently identified to contribute to sporadic Parkinson’s disease (PD) with dementia (PDD). Mice lacking interferon-beta (IFNβ) develop PDD-like disease; however, the phenotypic, cellular, and molecular impacts of IFNAR1 loss in vivo have not been explored. Studying cell-specific pathology in Ifnar1–/– mice may reveal potential disease-modifying therapeutic targets for PDD. Here, we present that Ifnar1–/– mice exhibit PDD-like pathogenesis, including dopaminergic neurodegeneration in the substantia nigra, Lewy-body-like alpha-synuclein+ inclusions, gliosis-associated phosphorylated-tau and amyloid-beta proteinopathy, and progressive PDD-like behavior deficits. Hallmark neuropathology and motor and cognitive behavior deficits were specifically recapitulated in mice lacking neuronal IFNAR1. Ifnar1–/– mice also exhibited early-onset nociceptive pain and neuropsychiatric abnormalities, recapitulated in mice lacking astrocytic IFNAR1. Neuron/astrocyte-specific transcriptomic and proteomic alterations in early-manifest Ifnar1–/– mice implicate synergistic dysfunctional excitatory neurotransmission upon IFNAR1 loss, leading to glucose hypermetabolism prior to cognitive decline. Targeted restoration of dysfunctional neuronal and astrocytic IFNAR1 could therefore potentially mitigate PDD progression through concerted regulation of excitatory neurotransmission.
2026-06-08 | PXD037113 | Pride
Project description:Comparison of gene expression in wildtype and MyD88-/- C57BL/6J mouse macrophages treated with 10 ng/mL LPS for 2 hours versus media treated control macrophages, and, wildtype and MyD88-/- C57BL/6J mouse macrophages treated with live E. coli bacteria (log phase; 1 bact per 1 macrophage) for 2 hours versus media treated control macrophages. Cells from 4 mice of each geneotype were used and each individual provided its own control. Hybridizations of treated and control samples from each mouse were dye swap replicated. Wildtype macrophages treated with LPS vs control (GSM22617-GSM22623,GSM22625), MyD88-/- macrophages treated with LPS vs control (GSM22626-GSM22632), wldtype macrophages treated with E. coli vs control (GSM22633-GSM22640, and MyD88-/- macrophages treated with E. coli vs control (GSM22641-GSM22648). Keywords: other
2004-05-16 | GSE1405 | GEO
Project description:Type I interferons (IFNs) are a family of cytokines that play an important role in regulating immune responses to pathogens and tumors and are used therapeutically. All IFNs are considered to signal via the heterodimeric IFNAR1-IFNAR2 complex, yet some subtypes such as IFN? can exhibit distinct functional properties, although the molecular basis of this is unclear. Here we demonstrate IFN uniquely and specifically ligates to IFNAR1 in an IFNAR2-independent manner and provide the structural basis of the IFNAR1-IFN interaction. We show that the IFNAR1-IFN complex transduces signals to modulate the expression of a set of genes independently of IFNAR2. Moreover, we show the in vivo importance of the IFNAR1-IFN signaling axis in a murine model of LPS-induced septic shock. Thus, we provide a molecular basis for understanding specific functions of IFN?. Interferon b induced gene expression in peritoneal exudate cells was measured 3hr post intra-peritoneal injection of 10,000IU/ml of interferon beta or saline into wildtype and Ifnar2-/- mice. Three independant experiments were performed for each treatment in both genotypes using different mice for each sample.
2013-07-13 | E-GEOD-48827 | biostudies-arrayexpress
Project description:Interferon-alpha/beta-receptor (IFNAR) signal defects were recently identified to contribute to sporadic Parkinson’s disease (PD) with dementia (PDD). Mice lacking interferon-beta (IFNβ) develop PDD-like disease; however, the phenotypic, cellular, and molecular impacts of IFNAR1 loss in vivo have not been explored. Studying cell-specific pathology in Ifnar1-/- mice may reveal potential disease-modifying therapeutic targets for PDD. Here, we present that Ifnar1-/- mice exhibit PDD-like pathogenesis, including dopaminergic neurodegeneration in the substantia nigra, Lewy-body-like alpha-synuclein+ inclusions, gliosis-associated phosphorylated-tau and amyloid-beta proteinopathy, and progressive PDD-like behavior deficits. Hallmark neuropathology and motor and cognitive behavior deficits were specifically recapitulated in mice lacking neuronal IFNAR1. Ifnar1-/- mice also exhibited early-onset nociceptive pain and neuropsychiatric abnormalities, recapitulated in mice lacking astrocytic IFNAR1. Neuron/astrocyte-specific transcriptomic and proteomic alterations in early-manifest Ifnar1-/- mice implicate synergistic dysfunctional excitatory neurotransmission upon IFNAR1 loss, leading to glucose hypermetabolism prior to cognitive decline. Targeted restoration of dysfunctional neuronal and astrocytic IFNAR1 could therefore potentially mitigate PDD progression through concerted regulation of excitatory neurotransmission.
2026-06-10 | GSE213671 | GEO
Project description:iCLIP of MATR3 from C57BL/6J wildtype mice
| PRJEB23795 | ENA
Project description:To elucidate the underlying immune responses elicited by IFNβ and GM-CSF-secreting CT2A cells to brain tumor microenvironment post resection compared to placebo group and non-IFNβ and GM-CSF-secreting CT2A cell group
2022-11-09 | GSE217253 | GEO
Project description:Type I interferons (IFNs) are a family of cytokines that play an important role in regulating immune responses to pathogens and tumors and are used therapeutically. All IFNs are considered to signal via the heterodimeric IFNAR1-IFNAR2 complex, yet some subtypes such as IFN? can exhibit distinct functional properties, although the molecular basis of this is unclear. Here we demonstrate IFN uniquely and specifically ligates to IFNAR1 in an IFNAR2-independent manner and provide the structural basis of the IFNAR1-IFN interaction. We show that the IFNAR1-IFN complex transduces signals to modulate the expression of a set of genes independently of IFNAR2. Moreover, we show the in vivo importance of the IFNAR1-IFN signaling axis in a murine model of LPS-induced septic shock. Thus, we provide a molecular basis for understanding specific functions of IFN?.
2013-07-13 | GSE48827 | GEO
Project description:Epstein-Barr virus (EBV) persistently infects over 90% of the human population and is the causative agent of infectious mononucleosis and human cancers. For the establishment of life-long infection, EBV tampers with the induction of type I interferon (IFN I)-dependent antiviral immunity in the host. How various EBV latency genes help orchestrate this crucial strategy is incompletely defined. Here, we reveal the mechanism by which the EBV nuclear antigen 3A (EBNA3A) inhibits IFNβ induction. Using proximity biotinylation we identify the histone acetyltransferase P300, a member of the IFNβ transcription complex, as a binding partner of EBNA3A. Follow-up experiments further demonstrate that EBNA3A also interacts with the activated IFN-inducing transcription factor IRF3 that collaborates with P300 in the nucleus and both events are mediated by the N-terminal domain of EBNA3A. Mechanistic studies reveal that EBNA3A reduces the binding of IRF3 to the IFNβ promotor, thereby hampering downstream IFN I signaling. These results reveal a novel mechanism by which viral immune evasion takes place.
2025-05-06 | PXD038572 | Pride
Project description:The current project is designed to evaluate the utility of proteomics in identifying pharmacodynamic (PD) biomarkers for biosimilarity assessment. This is an extension of the data submitted in GSE207945 which profiled longitudinal plasma samples from healthy subjects treated with single therapeutic doses/high doses of IFNβ-1a (30 μg) or Pegylated IFNβ-1a (125 μg) or placebo, to identify candidate PD biomarkers for the two biologics (n=248 for IFNβ-1a and N=528 for pegIFNβ-1a). The current project is a continuation study profiling longitudinal plasma samples from healthy subjects treated with a low dose of IFNβ-1a (7.5 μg) and pegIFNβ-1a (31.25 μg). In the current study, we reproduced the previous PD biomarker candidate responses at an intermediate/lower dose IFNβ-1a (15 μg) and pegIFNβ-1a (62.5 μg), and further characterized their PD response using characteristics such as significant area under the effect curve, dose-response, temporal profile and return to baseline, variability and sensitivity of the biomarker with sensitive doses on the steep portion of the dose-response curve and mechanism of action using the three tested dose-groups (high, intermediate and low) in the study.
2026-06-23 | GSE300489 | GEO