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10X single-cell RNASeq profiling of GP33-tetramer+ CD8+ T-cells from mice chronically infected with LCMV Clone 13

ABSTRACT: 10X single-cell RNASeq profiling of GP33-tetramer+ CD8+ T-cells from mice chronically infected with LCMV Clone 13

PROVIDER: PRJNA506056 | ENA |

REPOSITORIES: ENA

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10X single-cell RNASeq profiling of GP33-tetramer+ CD8+ T-cells from mice chronically infected with LCMV Clone 13

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

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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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RNA-Seq of CD8+ T cell subsets during LCMV infection [RNA-seq_D8_Brd4_KO]

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Identification of GP33-specific CD8 T cell clones responding to chronic infection with LCMV-Clone13

Project description:T cells specific for a certain antigen are a heterogeneous population characterized by cells expressing different T Cell Receptors (TCRs). As the TCR determines the avidity of a T cell clone for its cognate antigen, this feature has also a significant impact on the fate of such clone during antigenic challenge. In the context of chronic viral infection, T cells specific for the chronic virus differentiate into exhausted cells with limited functionality. We find that, in the process of exhaustion following infection with LCMV-Clone13, certain clones of CD8 T cells specific for the LCMV immunodominant epitope GP33 are enriched compared to others.

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Longitudinal expression data from CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD8+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-Db GP33-specific CD8+ T cells were sorted using MHC-I tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD8+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays

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10X single-cell RNASeq profiling of control or Ptpn2-null P14 CD8+ T-cells from mice chronically infected with LCMV Clone 13

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Project description:Chronic viruses and cancers thwart immune responses in humans by inducing T cell dysfunction. Using a murine chronic virus that models human infections, we investigated the function of the adhesion molecule, P-selectin glycoprotein ligand-1 (PSGL-1) that is upregulated on responding T cells. PSGL-1-deficient mice unexpectedly cleared the virus due to dramatic increases in the intrinsic survival of multifunctional effector T cells that had downregulated PD-1 and other inhibitory receptors. Notably, this response resulted in CD4+ T cell-dependent immunopathology. Mechanistically, PSGL-1 ligation on exhausted CD8+ T cells inhibited TCR and IL-2 signaling, and upregulated PD-1, leading to diminished survival with TCR stimulation. In models of malignant melanoma where T cell dysfunction occurs, PSGL-1-deficiency led to PD-1 downregulation, improved T cell responses, and tumor control. Thus, PSGL-1 plays a fundamental role in balancing viral control and immunopathology, and also functions as a checkpoint that regulates T cell responses in the tumor microenvironment. WT or PSGL-1 KO mice were infected with 2 x 10^6 PFU LCMV Clone 13. Spleens from 10 WT or 10 PSGL-1 KO animals were pooled and processed. CD8+ T cells were negatively enriched from WT or PSGL-1 KO spleens (EasySep Stemcell). Purified T cells were stained with propidium iodide (PI) for 10 minutes on ice, cells were washed. CD8+ T cells were stained with H2-Db-GP33-41 tetramers (NIH) and FACS sorted (BD FACS Aria). Sorted tetramer+ cells were PI negative and purity was >98%. Experiment was repeated twice to generate 2 WT (WT 1; WT 2) and 2 PSGL-1 KO (KO 1; KO 2) samples that represented 10 pooled spleens per sample.

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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: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

| PRJNA414459 | ENA

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