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The effect of type-I interferon signaling directly on CD8+ T cells following LCMV infection in the presence or absence of NK cells.

ABSTRACT: To understand the effect of type-I IFN signaling directly on CD8+ T cells following an LCMV infection we compared the overall gene expression of WT and Ifnar1-/- T cells following an LCMV infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE57355 | GEO | 2014/05/07

SECONDARY ACCESSION(S): PRJNA246323

REPOSITORIES: GEO

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The effect of type-I interferon signaling directly on CD8+ T cells following LCMV infection in the presence or absence of NK cells.

Project description:To understand the effect of type-I IFN signaling directly on CD8+ T cells following an LCMV infection we compared the overall gene expression of WT and Ifnar1-/- T cells following an LCMV infection. WT and Ifnar1-/- P14 cells were sorted from infected mice (day 3) that were depleted of NK cells or left untreated. Each sample and condition (WT or IFNAR) was performed in triplicates

2014-05-07 | E-GEOD-57355 | biostudies-arrayexpress

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Project description:Inhibition of IFN-I signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here we report that genetic ablation of IFNAR1 specifically in NK cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells, resulting in hastened virus clearance comparable to IFNAR1 blockade by an IFNAR1 neutralizing antibody. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell maturation, function, and killing of antigenspecific CD4 and CD8 T cells. Therefore, Inhibition of IFN I signaling in NK cells enhances CD4 and CD8 T cell responses, elevates humoral immune response, and thereby facilitates the control of persistent virus infection.

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NK cell regulation of T cells following LCMV infection of vaccinated and unvaccinated mice

Project description:NK cells may provide a “rheostat” function and have been shown to reduce the magnitude of antigen-specific T cell responses following infection. It remains unknown whether NK cells similarly modulate vaccine-elicited T cell responses following viral challenge. We used the LCMV clone 13 infection model to address whether NK cells regulate T cell responses in Adenovirus vector vaccinated mice following challenge. As expected, NK cell depletion in unvaccinated mice resulted in increased virus-specific CD4+ and CD8+ T cell responses and immunopathology following LCMV challenge. In contrast, NK cell depletion had minimal to no impact on antigen-specific T cell responses in mice that were vaccinated with an Ad5-GP vector prior to LCMV challenge. Moreover, NK cell depletion in vaccinated mice prior to challenge did not result in immunopathology and did not compromise protective efficacy. These data suggest that Adenovirus vaccine-elicited T cells may be less sensitive to NK cell-rheostat regulation than are T cells primed by LCMV infection.

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Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.

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Gene expression analysis of SMARTA in response to LCMV or Lm-gp61 infection

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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.

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Comparison of monocytic cells from naïve mice and day 14 LCMV Armstrong and day 14 LCMV Clone 13 infected mice

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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

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