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Gene expression profiles in GC B cells during acute and chronic viral infection

ABSTRACT: Gene expression profiles in GC B cells during acute and chronic viral infection

PROVIDER: PRJNA685826 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13261434.fastq.gz	Fastqsanger.gz
	SRR13261435.fastq.gz	Fastqsanger.gz
	SRR13261436.fastq.gz	Fastqsanger.gz
	SRR13261437.fastq.gz	Fastqsanger.gz
	SRR13261438.fastq.gz	Fastqsanger.gz

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Gene expression profiles in GC B cells during acute and chronic viral infection

Project description:To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, and RNA-seq was undertaken

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Chromatin accessibility regions in GC B cells during acute and chronic viral infection

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Gene expression profiles in GC B cells of wild-type and Bmi1 cKO mice during acute or chronic viral infection

Project description:To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type or Bmi1 conditional know-out in B cells mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, and RNA-seq was undertaken

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Gene expression profiles of CD4+CD25+ regulatory T cells during acute and chronic viral infection

Project description:Regulatory T (Treg) cells act as terminators in the case of T cell immunity during the acute phase of viral infection. However, their roles in chronic viral infection are not completely understood. We compared the phenotype and function of Treg cells during acute and chronic viral infection using lymphocytic choriomeningitis virus-infected mouse models. Chronic infection, unlike acute infection, led to induction of Treg cells and upregulation of various inhibitory receptors. Treg cells isolated from chronically infected mice (chronic Treg cells) displayed greater suppressive capacity for inhibiting T cell proliferation and subsequent cytokine production than those from naM-CM-/ve (naive Treg cells) or acutely infected mice (acute Treg cells). These gene expression profiles provided evidence that chronic Treg cells display characteristics distinct from either naive or acute Treg cells. Mouse splenic CD4+CD25+ regulatory T cells were analyzed at 0 day and 16 day after acute or chronic viral infection with LCMV Arm or CL13, respectively.

2014-12-05 | E-GEOD-63876 | biostudies-arrayexpress

Gene expression profiles of CD4+CD25+ regulatory T cells during acute and chronic viral infection

Project description:Regulatory T (Treg) cells act as terminators in the case of T cell immunity during the acute phase of viral infection. However, their roles in chronic viral infection are not completely understood. We compared the phenotype and function of Treg cells during acute and chronic viral infection using lymphocytic choriomeningitis virus-infected mouse models. Chronic infection, unlike acute infection, led to induction of Treg cells and upregulation of various inhibitory receptors. Treg cells isolated from chronically infected mice (chronic Treg cells) displayed greater suppressive capacity for inhibiting T cell proliferation and subsequent cytokine production than those from naïve (naive Treg cells) or acutely infected mice (acute Treg cells). These gene expression profiles provided evidence that chronic Treg cells display characteristics distinct from either naive or acute Treg cells.

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Gene expression profiles in GC B cells of wild-type and Bmi1 cKO mice during acute or chronic viral infection

Project description:Gene expression profiles in GC B cells of wild-type and Bmi1 cKO mice during acute or chronic viral infection

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Acute viral bronchiolitis

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Project description:Chronic CD8 T-cell stimulation in persisting infections or tumors can induce a stable gene expression program, known as T-cell dysfunction or exhaustion, that limits the cell’s effector functions and anti-viral and anti-tumor immunity. Thus far, the underlaying molecular mechanisms that induce and stabilize this phenotype are vaguely understood. We report here that establishing this program requires the thymocyte selection-associated high mobility group-box protein (Tox). Genetic disruption of Tox augments effector function, decreases the expression of PD-1, and significantly enhances immunopathology. These changes are linked to a failure in fixing the dysfunctional phenotype in the critical Tcf1+ progenitor population and to impaired epigenetic programing. Surprisingly, the gains in effector function co-incide with declining numbers of Tcf1+ cells and result ultimately in reduced total numbers of pathogen-specific T-cells. Thus, we establish Tox as a critical factor for the development of T-cell dysfunction and establish a clear link between CD8 T-cell intrinsic suppression of effector function and protection against immune-pathology. The terms acute and chronic samples refer to P14 T-cells that were initially activated in acute LCMV (Armstrong) or chronic LCMV (clone-13) infections. 4 weeks later, the P14 T cells were collected, transferred into naive mice, and both then re-expanded in acute LCMV (Armstrong) infection. 8 days later P14 T-cells were collected and analysed.

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