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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scATAC-Seq 2]

ABSTRACT: Longitudinal scATAC-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

ORGANISM(S): Mus musculus

PROVIDER: GSE199557 | GEO | 2022/10/31

REPOSITORIES: GEO

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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scATAC-Seq 1]

Project description:scATAC-seq from LCMV-specific P14 CD8 T cells after LCMV-Armstrong at day 60 and day 200 post infection

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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scRNA-seq and scATAC-seq coAssay]

Project description:Longitudinal scRNA-seq and scATAC-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scRNA-Seq]

Project description:Longitudinal scRNA-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

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Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [day 8 acute vs chronic]

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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miR-17~92 Regulates Effector and Memory CD8 T cell Fates by Modulating Proliferation in Response to Infection

Project description:miRNA profiling of Db-GP33-41 specific murine CD8 T cells following infection with LCMV Armstrong Various in-vivo subsets of antigen-specific CD8 T cells were FACS sorted and analyzed for miRNA expression profiling. Samples were purified from either uninfected animals or after days 4.5, 9 and >60 post infection with LCMV Armstrong.

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Early Transient IFN-γ Production-dependent and Independent Mechanisms Underlie the Cross-protectivity of Lung-Resident Memory CD8 T Cells against Respiratory Virus Challenge

Project description:Transcriptome profiling of lung tissues and lung CD8+ TRM during early phase of infection to investigate the mechanism of lung TRM cells during antigen re-exposure within 48hours. After P14 T cell transfer, PR8 infection would not induce P14 TRM cells, while PR8-gp33 would. Comparing the gene expression of lung tissues after LCMV Armstrong challenge at day 30 after PR8 or PR8-gp33 infection would help us understand the function of lung CD8+ TRM cells. Sorted TRM cells from mice challenged with LCMV Armstrong at day 30 after PR8-gp33 infection would reveal the activation mechanism of TRM cells.

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Gene expression profile of splenic p14 effector T cells eight days after LCMV infection

Project description:Microarray analyses was employed to determine the gene expression profiles of LCMV-specific p14 CD8+ effector T cells eight days after an acute LCMV Armstrong infection providing a framework to compare and contrast effector function potential of distinct immune cell subsets to CD8+ effector T cells.

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Expression Data from Memory P14 Tg CD8 T cells after either saline mock-infection, Pichinde Virus Infection (bystander infection) or Pichinde Virus infection with daily treatment with anti-CD122 (clone TM-b1)

Project description:Exposure to inflammatory cytokines driven by bystander cytokines can have profound effects on the function of memory CD8 T cells. Here we transferred a 1-5X10^4 of P14 TCR-tg T cells (specific for gp33-41 of LCMV) on day -1 followed by infection with 2X10^5 PFU of LCMV Armstrong ip to generate memory P14 populations. Mice were rested for >50 days before further challenge. Mice containing memory P14 populations were either mock-infected with saline, infected with 2X10^6 Pichinde Virus ip (no cross-reactivity wtih LCMV gp33-41) or infected with 2X10^6 Pichinde Virus ip together with daily injections of 200 micrograms of anti-CD122 antibody (clone TM-b1). On day 4 following indicated treatments P14s were flow sorted and RNA was extracted from 1X10^6 cells using an RNeasy kit (Qiagen). Each group had 3 biological replicates. Transcriptomes were compared by DAVID analysis (p<0.01, Fold-Change > 1.5) 3 biological replicates per group. Groups included P14 from mock-infected mice, P14 from Pichinde virus infected mice and P14 from Pichinde virus and anti-cd122 treated mice.

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RNA sequencing analysis of transferred C1qbp sufficient and deficient CD8+ T cells sorted from donor mice post infection with LCMV Armstrong

Project description:Tthis study is aimed to explore how C1qbp deficiency affects the mRNA expressing profiling during the differentiation stage of CD8+ T cells.Naïve WT and C1qbp KO P14 cells and transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 3, 5, 7 post-infection with LCMV Armstrong were collected and treated for RNA-seq. RNA-Seq analysis revealed transcriptomic changes between WT and C1qbp KO CD8+ T cells. Naïve WT and C1qbp KO CD8+ T cells showed similar gene expressing profiling. On day 3, 5, 7 post-infection with LCMV Armstrong, WT and C1qbp KO CD8+ T cells showed 341, 1,164 and 437 differentially expressed genes respectively.

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