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Gene expression changes in in vitro equivalents of DC progenitors from uninfected or LCMV Cl13-infected mice upon Gmeb1 knockdown and treatment with glucocorticoid

ABSTRACT: Gene expression changes in in vitro equivalents of DC progenitors from uninfected or LCMV Cl13-infected mice upon Gmeb1 knockdown and treatment with glucocorticoid

PROVIDER: PRJNA786961 | ENA |

REPOSITORIES: ENA

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Gene expression changes in in vitro equivalents of DC progenitors from uninfected or LCMV Cl13-infected mice upon Gmeb1 knockdown and treatment with glucocorticoid

Project description:Gmeb1 and glucocorticoids suppress pDC development. To address which genes are involved in regulation of pDC development downstream of Gmeb1 and/or glucocorticoids, we investigated the gene expression profiles of pro-DCs (in vitro equivalents of DC progenitors) from bone marrow Flt3L culture from uninfected or LCMV Cl13-infected mice after knockdown of Gmeb1 or treatment with corticosterone.

2024-12-07 | GSE190408 | GEO

Pair-feeding of LCMV Cl13 infected mice

Project description:Mice were infected with LCMV Cl13 and food intake was measured up to 8dpi. Another group of uninfected mice received the amount of food the infected mice consumed. The third group of naïve mice received food ad libitum.

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Naïve and LCMV Cl13 infected liver tissue of ERT2 AlbCre Ifnar1 fl/fl mice

Project description:Age- and sex-matched (male, 2-3 months old) ERT2 AlbCre Ifnar fl/fl and ERT2 AlbCre Ifnar +/+ mice were injected intraperitoneally with 40 mg/kg tamoxifen for 5 consective days. Mice were then intravenously infected with 2x10^6 focus forming units of LCMV Cl13 and liver tissue of either genotype was harvested 1.5 days post infection and analyzed for transcriptomic changes (n = 3). Liver tissue of uninfected animals of both genotypes was harvested as control (n = 3).

2019-12-05 | GSE117237 | GEO

Bulk RNA seq of intestinal immune cells from naïve, LCMV-Arm and LCMV-Cl13 infected mice

Project description:We report that the gastrointestinal tract (GIT) is a previously unappreciated long-term reservoir of chronic LCMV-Cl13 infection, and, chronic viral replication in the GIT has a profound effect on the local immune compartment as well as the development of subsequent immune responses. CD45+ immune cells were sorted and analyzed by RNAseq from the small and large intestines of naive mice, or mice infected 30 days prior with LCMV-Arm (acute virus) or LCMV-Cl13 (chronic virus). We show that GIT immune cells from acute and chronically infected mice differ substantially from naive mice; chronically infected mice show increases in genetic pathways involved in T cell activation and killing, inflammasome activation and interferon signaling; chronically infected mice show reduced expression of genes involved in T cell memory and antigen presenting cell activation; and chronic infection induces metabolic changes unique to the small but not large intestinal immune compartment.

2020-08-11 | GSE142303 | GEO

Pair-feeding of LCMV Cl13 infected mice

Project description:Pair-feeding of LCMV Cl13 infected mice

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Gene expression changes in liver upon LCMV Cl13 infection

Project description:Gene expression changes in liver upon LCMV Cl13 infection

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Gene expression changes in liver upon LCMV Cl13 infection.

Project description:2-3 month old female C57Bl/6J mice were intravenously infected with 2x10^6 focus forming units of lymphocytic choriomeningitis virus strain Clone-13. Whole liver tissue was harvested in duplicated from uninfected control mice, uninfected 123d old mice, and from infected at 2, 8, 30, 60, and 123 days post infection. Three TMT 6-plex runs were carried out to monitor the changes in liver protein abundance during the entire course of infection. The first run included samples from day 2 and day 8 after infection along with the uninfected controls. Similarly, the second run included uninfected controls and samples from day 30 and day 60 after infection. The third run included samples day 123 after infection, the corresponding age matched control that was left uninfected for 123 days and the uninfected controls used in the other two runs. The uninfected controls were included in all the three runs as an internal control to monitor reproducibility between the runs.

2019-12-02 | PXD011122 | Pride

Bulk RNA seq of intestinal immune cells from naïve, LCMV-Arm and LCMV-Cl13 infected mice

Project description:Bulk RNA seq of intestinal immune cells from naïve, LCMV-Arm and LCMV-Cl13 infected mice

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RNA-seq of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of persistent LCMV-Clone 13 viral infection

Project description:Altered CD8 T cell differentiation and functional exhaustion prevent control of chronic virus infection and cancer. Yet, how fate commitment and exhaustion are determined and dynamically modulated throughout persistent infection are unclear. We compared the activation and differentiation of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of established persistent LCMV-Clone 13 viral infection. LCMV GP33-specific CD8 TCR transgenic (P14) cells were injected into naïve mice immediately infected with LCMV-Cl13 (Early priming) or into mice that had been infected 21 days earlier with LCMV-Cl13 (Late Priming). Sixty hours post-priming P14 cells were sorted from mice and subjected to RNA seq. We show early primed cells very rapidly exhibit a transcriptional profile of robust activation, effector differentiation and dysfunction, while late primed cells have increased expression of genes involved in memory differentiation and maintenance.

2018-10-09 | GSE105044 | GEO

Gene expression profile analysis of mouse whole spleen following infection by lymphocytic choriomeningitis virus (LCMV), comparing LCMV-Armstrong and LCMV-Clone 13 expression patterns at 0, 5, 9, and 30 days

Project description:To identify mechanisms behind immunosuppression during virus infections, we infected mice with LCMV-Armstrong and LCMV-Clone 13 expression patterns. LCMV-Armstrong induces a T-cell reaction that resolves infection within 8-10 days, while LCMV-Clone13 generates a persisten infection through immunosuppression. We used microarray to uncover splenic gene expression patterns specific to each LCMV infection at 5, 9, and 30 days C57BL6 mice, 6-10 weeks old, were infected with LCMV-Armstrong and LCMV-Clone 13 or left uninfected (naïve). At days 5, 9, and 30 whole spleens were harvested for RNA extraction and hybridization on Affymetric microarray.

2013-02-15 | E-GEOD-44322 | biostudies-arrayexpress

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