Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260167 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The mass spectrometry data describes the phosphorylation of a transcription factor known as interferon regulatory factor 9 (IRF9), under IFNbeta-induced or non-induced conditions. IRF9 is involved in the transcriptional regulation of hundreds of interferon-stimulated genes as part of the innate immune response.
2022-07-20 | MSV000089924 | MassIVE
Project description:Wang et al. identify MARK2 as a key regulator of innate antiviral immunity. The phosphorylation of GEF-H1 at Ser645 by MARK2 enhances TBK1 activation and induces IFN-β and interferon-stimulated genes. This establishes the MARK2–GEF-H1–TBK1 axis as a fundamental component of host antiviral defense.
2025-12-15 | PXD071998 |
Project description:Innate immune responses induce hundreds of interferon-stimulated genes (ISGs), many of which play an important role in antiviral immunity. Viperin, a member of the radical SAM superfamily of enzymes, is the product of one such ISG and it restricts the replication of a broad spectrum of DNA and RNA viruses. However, a general mechanism that explains all the roles proposed for viperin in the innate immune response remains to be defined. Here we report a previously unknown antiviral mechanism, in which viperin represses translation of viral RNA. We show that viperin interacts with the translation machinery and, primarily through its radical SAM enzymatic activity, inhibits global translation during the interferon response by activating the eIF2 pathway. In cell based-infection assays, viperin inhibits viral protein synthesis and viral replication of Zika virus and Kunjin virus. This study illustrates the importance of translational repression in the antiviral response and identifies viperin as a central translational regulator in innate immunity.
2022-05-22 | GSE142015 | GEO
Project description:Wild type HIV-1 can infect macrophages to establish productive infection without triggering innate immune receptors or type 1 interferon responses that would otherwise restrict virus propagation. We found that HIV-1 capsid mutants that disrupt capsid interactions with two host factors CPSF6 and cyclophillin A do not replicate in macrophages because they do trigger interferon responses. Genome-wide transcriptional profiling was used to compare the repertoire of interferon stimulated genes induced by these capsid mutants after 24Êh with stimulation of macrophages with interferon-beta or with the RNA analogue Poly IC.
2014-02-12 | E-MTAB-1437 | biostudies-arrayexpress
Project description:Amyloid beta (Aβ) plaque deposition in the central nervous system (CNS) is a hallmark of Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA), triggering an innate immune response. However, the role of the adaptive immune system is less clear. We investigated immune microenvironment dynamics in APP23 transgenic (APP23-tg) mice modelling CNS amyloid pathology, using single-cell transcriptomics. A significant increase in T-cell populations, particularly CD8+ T-cells, was observed in late stages, clustering around Aβ plaques, indicating a targeted response. A novel Aβ plaque-associated subset of CD8+ T-cells expressing interferon-stimulated genes (ISGs), was found to drive Type-I interferon responses. This subset also produced CXCL10, which mediated non-ISG T-cell trafficking via the CXCL10-CXCR3 axis. Importantly, we corroborated our observations by identifying similar Type-I interferon responses near plaques in human CNS amyloid pathology. These findings highlight a shift from microglia-driven to T-cell-mediated neuroinflammation as amyloid pathology progresses, with implications for time-resolved therapy development.
2026-01-01 | GSE280018 | GEO
Project description:The study shows that RLRs drive distinct immune gene activation and polarization of the immune response. In our data, the RLR-dependent, WNV-induced immune response polarization overshadows the classical drivers of viral innate immune responses, interferon I (IFN) and IFN-stimulated genes, thus underscoring the importance of innate immune activation for channeling the adaptive immune system into specific effector pathways
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Project description:Dendritic cells (DC) play a pivotal regulatory role in activation of the innate as well as the adaptive part of the immune system by responding to environmental microorganisms. We have previously shown that some lactobacilli strains induce a strong production of the pro-inflammatory and Th1 polarizing cytokine IL-12 in DC. Contrary, bifidobacteria do not induce IL-12, but are able to inhibit the IL-12 production induced by lactobacilli. In the present study, genome wide microarrays were used to investigate the maturation and gene expression pattern murine bone marrow derived DC stimulated with Lactobacillus acidophilus NCFM and Bifidobacterium bifidum Z9. L. acidophilus NCFM strongly induced expression of interferon (IFN)-β, multiple virus defence genes, and cytokine and chemokine genes related to both the adaptive and the innate immune response. Contrary, B. bifidum Z9 mostly up-regulated genes encoding cytokines and chemokines related to the innate immune response. Moreover, B. bifidum Z9 inhibited the expression of the genes initiating the adaptive immune response induced by L. acidophilus NCFM and had an additive effect on genes of the innate immune response and some Th2 skewing genes. The gene encoding Jun dimerization protein 2 (JDP2), a key regulator in cell signalling, was one of the few genes only induced by B. bifidum Z9. Blocking of the JNK1/2 pathway completely inhibited the gene expression of Ifn-β. We suggest that B. bifidum Z9 employs an active mechanism to inhibit induction of genes in DC triggering the adaptive immune system and that JPD2 is involved in the regulatory mechanism. In the experiment saline control, Lactobacillus acidophilus NCFM, Bifidobacterium bifidum Z9 or both bacteria were were added to murine dendritic cells and stimulated for 10 hours. Experiments were run in triplicates and analyzed in a Two-way ANOVA design.
2010-02-24 | E-GEOD-20302 | biostudies-arrayexpress
Project description:Dendritic cells (DC) play a pivotal regulatory role in activation of the innate as well as the adaptive part of the immune system by responding to environmental microorganisms. We have previously shown that some lactobacilli strains induce a strong production of the pro-inflammatory and Th1 polarizing cytokine IL-12 in DC. Contrary, bifidobacteria do not induce IL-12, but are able to inhibit the IL-12 production induced by lactobacilli. In the present study, genome wide microarrays were used to investigate the maturation and gene expression pattern murine bone marrow derived DC stimulated with Lactobacillus acidophilus NCFM and Bifidobacterium bifidum Z9. L. acidophilus NCFM strongly induced expression of interferon (IFN)-β, multiple virus defence genes, and cytokine and chemokine genes related to both the adaptive and the innate immune response. Contrary, B. bifidum Z9 mostly up-regulated genes encoding cytokines and chemokines related to the innate immune response. Moreover, B. bifidum Z9 inhibited the expression of the genes initiating the adaptive immune response induced by L. acidophilus NCFM and had an additive effect on genes of the innate immune response and some Th2 skewing genes. The gene encoding Jun dimerization protein 2 (JDP2), a key regulator in cell signalling, was one of the few genes only induced by B. bifidum Z9. Blocking of the JNK1/2 pathway completely inhibited the gene expression of Ifn-β. We suggest that B. bifidum Z9 employs an active mechanism to inhibit induction of genes in DC triggering the adaptive immune system and that JPD2 is involved in the regulatory mechanism.
2010-02-13 | GSE20302 | GEO
Project description:Using a unique model of cultured human beta cell senescence we show that chromatin reorganization leads to activation of enhancers regulating functional maturation genes, concomitantly with acquisition of glucose-stimulated insulin secretion capacity. Interferon-response genes are elevated in senescent beta cells, but cytokine-encoding senescence-associated secretory phenotype (SASP) genes are not. Human beta cell senescence thus involves chromatin-driven upregulation of a functional maturation program and of interferon-stimulated genes, changes that could increase both insulin secretion and immune reactivity.
2024-06-26 | GSE207818 | GEO
Project description:Using a unique model of cultured human beta cell senescence we show that chromatin reorganization leads to activation of enhancers regulating functional maturation genes, concomitantly with acquisition of glucose-stimulated insulin secretion capacity. Interferon-response genes are elevated in senescent beta cells, but cytokine-encoding senescence-associated secretory phenotype (SASP) genes are not. Human beta cell senescence thus involves chromatin-driven upregulation of a functional maturation program and of interferon-stimulated genes, changes that could increase both insulin secretion and immune reactivity.
2024-06-26 | GSE207816 | GEO