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Kinetics of Tbet+ B cells during LCMV infection

ABSTRACT: Kinetics of Tbet+ B cells during LCMV infection

PROVIDER: PRJNA793040 | ENA |

REPOSITORIES: ENA

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Kinetics of Tbet+ B cells during LCMV infection

Project description:Kinetics of Tbet+ B cells during LCMV infection

| PRJNA631250 | ENA

Kinetics of Tbet+ B cells during LCMV infection

Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.

2022-01-27 | GSE192765 | GEO

Kinetics of Tbet+ B cells during LCMV infection

2022-01-27 | GSE150139 | GEO

Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. NaÃ¯ve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection

2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress

LCMV-Armstrong infection

Project description:LCMV-Armstrong infection

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Whole mouse genome analysis of LCMV-specific CD4 and CD8 T cells throughout acute and chronic LCMV infection.

Project description:CD4 and CD8 T cells display functional defects during chronic infection such as loss of certain cytokines. Recent studies have suggested that CD4 T cells may actually gain other functions, however. Here, we analyzed gene expression profiles from LCMV-specific CD4 and CD8 T cells throughout the response to either acute LCMV or chronic LCMV infection. This alllowed us to identify CD4-specific changes during chronic infection compared to acute infection but also revealed shared core regulators between CD4 and CD8 T cells. LCMV-specific CD4 and CD8 T cells were isolated 6, 8, 15 and 30 days post infection with LCMV Armstrong or LCMV clone 13. Naïve CD4 and CD8 T cells were also isolated from naïve mice as comparisons. Four replicates of each sample were hybridized. The only exception is LCMV-specific CD4 T cells isolated 6 days post infection with LCMV-Arm where only three replicates were hybridized.

2012-12-12 | E-GEOD-30431 | biostudies-arrayexpress

P14 CD8 T cells during acute LCMV infection

Project description:P14 CD8 T cells during acute LCMV infection

| PRJNA632045 | ENA

Primary and secondary CD8 T cells during acute and chronic LCMV infection

Project description:Understanding the response of memory CD8 T cells to persistent antigen re-stimulation and the role of CD4 T cell help is critical to the design of successful vaccines for chronic diseases. However, studies comparing the protective abilities and qualities of memory and naïve cells have been mostly performed in acute infections, and little is known about their roles during chronic infections. Herein, we show that memory cells dominate over naïve cells and are protective when present in large enough numbers to quickly reduce infection. In contrast, when infection is not rapidly reduced, memory cells are quickly lost, unlike naïve cells. This loss of memory cells is due to (i) an early block in cell proliferation, (ii) selective regulation by the inhibitory receptor 2B4, and (iii) increased reliance on CD4 T cell help. These findings have important implications towards the design of T cell vaccines against chronic infections and tumors. 16 samples are analyzed: 3 replicates of secondary effector CD8 P14 T cells at day 8 post-acute lymphocytic choriomeningitis virus (LCMV) infection; 4 replicates of secondary effector CD8 P14 T cells at day 8 post-chronic LCMV infection; 4 replicates of primary effector CD8 P14 T cells at day 8 post-acute LCMV infection; and 5 replicates of primary effector CD8 P14 T cells at day 8 post-chronic LCMV infection.

2011-08-22 | E-GEOD-30962 | biostudies-arrayexpress

RNA-Seq of CD8+ T cells during LCMV infection [WT infection]

Project description:RNA-Seq of CD8+ T cells during LCMV infection [WT infection]

| PRJNA436006 | ENA

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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