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

ABSTRACT: miRNA profiling of Db-GP33-41 specific murine CD8 T cells following infection with LCMV Armstrong

ORGANISM(S): Mus musculus Rattus norvegicus Betapolyomavirus hominis Human alphaherpesvirus 1 JC polyomavirus Betapolyomavirus macacae Human gammaherpesvirus 8 Homo sapiens Human immunodeficiency virus 1 human gammaherpesvirus 4 Human betaherpesvirus 5

PROVIDER: GSE46052 | GEO | 2013/04/16

SECONDARY ACCESSION(S): PRJNA197136

REPOSITORIES: GEO

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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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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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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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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]

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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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