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Bulk RNA sequencing of DGKa deficient and wildtype P14 CD8 T cells after LCMV Clone 13 infection

ABSTRACT: Bulk RNA sequencing of DGKa deficient and wildtype P14 CD8 T cells after LCMV Clone 13 infection

PROVIDER: PRJNA773081 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16504300_1.fastq.gz	Fastqsanger.gz
	SRR16504300_2.fastq.gz	Fastqsanger.gz
	SRR16504301_1.fastq.gz	Fastqsanger.gz
	SRR16504301_2.fastq.gz	Fastqsanger.gz
	SRR16504302_1.fastq.gz	Fastqsanger.gz

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Bulk RNA sequencing of DGKa deficient and wildtype P14 CD8 T cells after LCMV Clone 13 infection

Project description:exposure to LCMV Clone 13 infection in the absence of DGKa leads to excessive inflammation and mortality

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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.

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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.

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Project description:Four distinct populations of exhausted CD8+ T-cells occur in chronic LCMV Clone 13 infection

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Areas of H3K27 tri-methylation in CD8+ T cells from the spleens of LCMV-Armstrong or LCMV-Clone 13 infected mice

Project description:The profiles of H3K27 tri-methylation in CD8+ T cells from LCMV-Armstrong and LCMV-Clone 13 infected mice are known to be distinct from one another. We used CUT&RUN (Cleavage Under Targets and Release Using Nuclease) to analyze these differences in splenic CD8+ T cells of these two infection conditions.

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Gene expression profiles at the single cell level of CD8+ T cells from the spleens of LCMV-Armstrong or LCMV-Clone 13 infected mice

Project description:The transcriptomes of CD8+ T cells from LCMV-Armstrong and LCMV-Clone 13 infected mice are known to be distinct from one another. We used single cell RNA sequencing (scRNA-seq) to analyze the transcriptomic diversity of splenic CD8+ T cells in these two infection conditions at various timepoints after infection.

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