Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA190692 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNA-155 (miR-155) is upregulated in primary effector CD8 T cells but is expressed at low amounts in naïve cells. Anti-viral CD8 T cell responses and viral clearance were impaired in miR-155 deficient (bic-/-) mice, and this defect was intrinsic to CD8 T cells, as adoptively transferred bic-/- CD8 T cells generated greatly reduced primary and memory responses during infection. To understand the mechanism by which miR-155 regulates CD8 T cell activation, we analyzed the gene expression profiles of naive and in vitro activated wild-type and bic-/- CD8 T cells.
2013-02-26 | GSE44649 | GEO
Project description:MicroRNA-155 (miR-155) is upregulated in primary effector CD8 T cells but is expressed at low amounts in naïve cells. Anti-viral CD8 T cell responses and viral clearance were impaired in miR-155 deficient (bic-/-) mice, and this defect was intrinsic to CD8 T cells, as adoptively transferred bic-/- CD8 T cells generated greatly reduced primary and memory responses during infection. To understand the mechanism by which miR-155 regulates CD8 T cell activation, we analyzed the gene expression profiles of naive and in vitro activated wild-type and bic-/- CD8 T cells. CD8 T cells were purified from uninfected C57BL/6 mice and stimulated in vitro with plate-bound anti-CD3 and anti-CD28 antibodies for 48 h or left unstimulated. RNA from these CD8 T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays.
2013-02-26 | E-GEOD-44649 | biostudies-arrayexpress
Project description:To study effect of VRK1 deletion on spermatogenesis of the mouse, transciptomic analysis of genes in postnatal 8-day testicular cells of wild type and VRK1-deficient Mus musculus was performed.
2011-12-30 | GSE22674 | GEO
Project description:The microRNA (miRNA) dependent regulation of gene expression confers robustness to cellular phenotypes and controls responses to extracellular stimuli. Although a single miRNA can regulate expression of hundreds of target genes, it is unclear whether any of its distinct biological functions can be due to the regulation of a single target. To explore in vivo the function of a single miRNA-mRNA interaction, we mutated the 3' UTR of a major miR-155 target SOCS1 to specifically disrupt its regulation by miR-155. We found that under physiologic conditions and during autoimmune inflammation or viral infection some immunological functions of miR-155 were fully or largely attributable to the regulation of SOCS1, whereas others could be accounted only partially or not at all by this interaction. Our data suggest that the role of a single miRNA-mRNA interaction is cell type- and biological context-dependent. Naive WT, SOCS1KI and miR-155KO OVA-specific OT-1 TCR transgenic CD8+ T cells (1x10e4 per mouse) were adoptively transferred into CD45.1+ wt mice prior to infection with MCMV-OVA. WT, SOCS1KI and miR-155KO NK cells (2x10e5 per mouse) were adoptively transferred into CD45.1+ Klra8KO (Ly49H-deficient) mice prior to infection with MCMV. On d4 post infection, CD45.2+ CD44+ CD8+ OT-1 and CD45.2+ Ly49H+ NK1.1+ CD3- NK cells were FACS-sorted (BD FACS ARIA2). Each condition has 3 sequencing replicates.
2015-05-10 | E-GEOD-68511 | biostudies-arrayexpress
Project description:The microRNA miR-155 is essential for CD8+ T cell antiviral and antitumor immunity but the mechanisms behind its activity remain unresolved. Here, we show that miR-155 increased CD8+ T cell antitumor function by restraining T cell senescence and functional exhaustion through epigenetic silencing of key drivers of effector differentiation. miR-155 enhanced the function of polycomb repressor complex 2 (PRC2) indirectly by promoting the expression of the PRC2 cofactor Phf19 via AKT signaling. Phf19 orchestrated a transcriptional program extensively shared with miR-155 to enhance T cell engraftment, polyfunctionality, and antitumor immunity. These effects were dependent on the histone-binding capacity of Phf19 which is critical for the PRC2 recruitment to chromatin. These findings establish miR-155–Phf19–PRC2 as a pivotal axis regulating CD8+ T cell differentiation. Targeting the microRNA–polycomb-group protein circuitry is a promising route to potentiate cancer immunotherapy through epigenetic reprogramming of CD8+ T cell fate.
2019-03-08 | GSE99801 | GEO
Project description:The microRNA miR-155 is essential for CD8+ T cell antiviral and antitumor immunity but the mechanisms behind its activity remain unresolved. Here, we show that miR-155 increased CD8+ T cell antitumor function by restraining T cell senescence and functional exhaustion through epigenetic silencing of key drivers of effector differentiation. miR-155 enhanced the function of polycomb repressor complex 2 (PRC2) indirectly by promoting the expression of the PRC2 cofactor Phf19 via AKT signaling. Phf19 orchestrated a transcriptional program extensively shared with miR-155 to enhance T cell engraftment, polyfunctionality, and antitumor immunity. These effects were dependent on the histone-binding capacity of Phf19 which is critical for the PRC2 recruitment to chromatin. These findings establish miR-155–Phf19–PRC2 as a pivotal axis regulating CD8+ T cell differentiation. Targeting the microRNA–polycomb-group protein circuitry is a promising route to potentiate cancer immunotherapy through epigenetic reprogramming of CD8+ T cell fate.
2019-03-11 | GSE99918 | GEO
Project description:Sequencing of tumor associated (B16f10-OVA) mir-155 Wt or deficient CD4+ and CD8+ T cells
| PRJNA395212 | ENA
Project description:Expression data of wild type and miR-155 knockout bone marrow derived dendritic cells treated with lipopolysaccharide (LPS)
| PRJNA130951 | ENA
Project description:To study effect of VRK1 deletion on spermatogenesis of the mouse, transciptomic analysis of genes in postnatal 8-day testicular cells of wild type and VRK1-deficient Mus musculus was performed. Gene expression in testes from from wild type and VRK1-deficient mutant Mus musculus, respectively, was measured. Four independent experiments for wild type and mutant, respectively, were performed.
2011-12-30 | E-GEOD-22674 | biostudies-arrayexpress
Project description:Classically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages.
2016-07-15 | GSE77425 | GEO