Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA315273 | ENA |
REPOSITORIES: ENA
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Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-α in vitro and that Siglec-H ko mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed
2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress
Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-α in vitro and that Siglec-H ko mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease.
2016-03-16 | GSE79248 | GEO
Project description:Murine Cytomegalovirus (MCMV) infection leads to early activation of various immune cells, including B and T lymphocytes, before the actual initiation of antigen-specific adaptive immunity. This activation is partly driven by innate cytokines, including type I interferon (IFN), which are induced early after infection. The objective of this study was to address the role of type I IFN in shaping early/innate B and T cell responses to a primary acute viral infection. In order to decipher the specific impact of IFN-I on cell subsets, we performed a genome-wide expression analysis on WT splenic B and CD8 T lymphocytes isolated from C57BL/6 [CD45.1 WT / CD45.2 IFNAR-KO] mixed bone marrow chimera mice. This study complements series GSE39555, which focused on early responses of NK cells and of the two subsets of conventional dendritic cells. This study includes data from B and CD8 T lymphocytes purified by flow cytometry sorting from the spleen of bone marrow chimera (BMC) mice, under steady-state or MCMV conditions. Two independent replicates were made for each cell type, from two independent pools of spleens from uninfected or d1.5 MCMV-infected BMC 5-8 mice, and were hybridized on 3 separate batches of GeneChips.
2013-04-03 | E-GEOD-45365 | biostudies-arrayexpress
Project description:The transcriptomes of FACS-sorted siglec-F+ alveolar macrophages and siglec-f- CD11b+ exudative macrophages from inducible airway GM-CSF over-expressing transgenic mice (DTGM) were compared to non-inducible littermate controls during influenza A virus infection.
2018-01-12 | GSE109099 | GEO
Project description:Lung gene expression after long-term (26 weeks, 52 weeks, 78 weeks & 104 weeks) styrene inhalation exposure at a single concentration (120ppm) in three strains of C57BL/6 mice -- wild-type (WT), CYP2F2 knockout (KO), and CYP2F1 humanized (TG) mice, and CD-1 mice. These data examine transcriptomic changes in lung tissue after long-term styrene inhalation in male C57Bl/6 and CD-1 mice. Styrene causes increased lung tumors in mice, but not in rats. Mouse lung tumors were found mostly at the conclusion of a life-time (104 weeks for males) exposure study and most were benign. Styrene is largely negative in genotoxicity assays. Styrene metabolism by CYP2F2 produced a different metabolite pattern in mouse lung than in liver or in rats or humans. The purpose of this study was to use genomic analyses to further investigate potential modes of action (MoA) of styrene in mice after long-term exposure to styrene. Mice strains exposed were C57BL/6 wild-type (WT), CYP2F2 knockout (-/-; KO) and CYP2F21 humanized transgenic (2F2-KO + 2F1,2A13,2B6-transgenic, TG), and CD-1 male mice using 120 ppm styrene at 6 hr/day 5 days/wk for 26, 52, 78 and 104 weeks. Lungs were analyzed by Affymetrix whole genome microarrays for each strain relative to sample time-specific vehicle controls for each strain.
2018-03-08 | GSE98470 | GEO
Project description:Hepatocyte Nuclear Factor 4 alpha (HNF4α), a master regulator of hepatocyte differentiation, and circadian regulator Aryl Hydrocarbon-Like Receptor-Like 1 (ARNTL, or BMAL1) though robustly co-expressed in healthy liver, are incompatible within the context of HCC. Differential expression of Bmal1 and Hnf4α may control susceptibility to liver disease and ultimately, hepatocellular carcinoma. We compared gene expression profiles under conditions of inducible loss of hepatic Hnf4α and inducible loss of Hnf4a and Bmal1 in this RNA-seq experiment. Hepatic Hnf4a (H-KO) or Hnf4a and Bmal1 (BH-KO) were inducibly knocked out after 5 days tamoxifen treatment in eight week-old mice (H-KO) or (BH-KO) followed by vivarium chow or high fat feeding (BH-HF-KO). Littermate control mice (H-WT, BH-WT and BH-HF-WT ) were also treated with tamoxifen at eight weeks of age, but since they lacked the Cre transgene, Hnf4a and Bmal1 expression remained intact. Livers were harvested at 10 weeks of age (BH-WT/KO, H-WT/KO) or 45 weeks ( BH-HF-WT/KO) of age after high fat diet feeding, and liver tissue was flash frozen in liquid nitrogen.
2022-08-01 | GSE173968 | GEO
Project description:ADAR1 is an interferon (IFN) inducible RNA editing enzyme that converts adenosine (A) to inosine (I). Here we identified ADAR1 and ADAR1p150 specific editing events by conducting RNA-seq on WT, ADAR1 KO, and ADAR1p150 KO cells.
2018-02-09 | GSE99249 | GEO
Project description:Murine Cytomegalovirus (MCMV) infection leads to the activation of various immune cells, including dendritic cells (DCs) and Natural Killer (NK) cells. This activation is partly driven by innate cytokines including IFN-I, which are induced early after infection. The objective was to address the role of different innate cytokines in shaping DC subsets and NK cell responses, in particular the role of cell intrinsic responses to IFN-I. In order to decipher the specific impact of cell-intrinsic IFN-I on cell subsets, we performed a genome-wide expression analysis on CD45.1 WT and CD45.2 IFNAR-/- splenic conventional DC (cDC) subsets and NK cells isolated from C57BL/6 [CD45.1 WT / CD45.2 IFNAR-KO] mixed bone marow chimera mice. This study includes data from cDC subsets (CD8a and CD11b) and NK cells purified by flow cytometry sorting from the spleen of bone marrow chimera (BMC) mice, under steady-state or MCMV condition. Two independent replicates were made for each cell type, from two independent pools of spleens from uninfected or d1.5 MCMV-infected BMC 5-8 mice, and were hybridized on 3 separate batches of gene chips.
2012-10-17 | E-GEOD-39555 | biostudies-arrayexpress
Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers, airway organoids, and alveolar organoids and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT). Technical triplicates of ∆Np63 WT and ∆Np63 KO were harvested for each growth condition for RNA sequencing.
2022-11-11 | GSE216160 | GEO
Project description:Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. We knocked out (using the inducible AhCre-LoxP system) Polycomb genes Eed and Ezh2 in the intestine for 6 weeks, after which crypts - the small intestinal stem cell zone - were harvested and RNA sequenced. We found Wnt, Notch and cell cycle pathways to be affected in Eed knockout (KO) but not Ezh2 KO crypts. Direct targets of Eed were determined by comparing this data with ChIP-sequencing. Small intestinal crypt mRNA profiles of 6 weeks-induced 12 weeks old Eed KO, Ezh2 KO and WT mice (all triplicates) as well as 10 days-induced Eed KO and WT organoids (duplicates) were generated by RNA sequencing over two runs and using IlluminaHiseq2000 and Hiseq2500.
2016-07-01 | E-GEOD-81576 | biostudies-arrayexpress