Project description:This SuperSeries is composed of the following subset Series: GSE18524: Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells GSE18525: Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells Refer to individual Series
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. Naïve mouse CD4 T spleenocytes with VIP ligand (sample) vs. naïve mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP.
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. PMA/ionomycin (activated) mouse CD4 T spleenocytes with VIP ligand (sample) vs. PMA/ionomycin (activated) mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP.
Project description:Transcriptome analysis to investigate the effects of the smac mimetic AT406 on the differentiation of murine Th17 cells compared to DMSO controls, and to investigate the transriptome of murine Th17 cells compared to control undifferentiated naive CD4 T cells.
Project description:Although HIV-1 can directly infect resting CD4+ T cells, virus replication in resting CD4+T cells is very inefficient owing to the different host restriction factors blocking viral replication. The accessory protein Vpx from the major simian immunodeficiency virus (SIV) of rhesus macaque (mac) and HIV-2 lineage could degrade a host restriction factor, SAM and HD domain containing protein 1 (SAMHD1), to facilitate HIV reverse transcription. Interestingly, Vpx proteins from a second SIV lineage, the SIV of redcapped mangabeys or mandrills (SIVrcm/nmd-2), had no effect on SAMHD1 and did not affect the dNTP pool, but strongly increased HIV-1 infection in resting CD4+ T cells although not in primary macrophages. This indicates that Vpx, in addition to SAMHD1,can overcome a previously unexplored restriction factor for lentiviruses. Here to identify this potential restriction factor, we examined Vpxrcm-interacting cellular proteins and found that keratin 72 (KRT72), an intermediate filament protein that is exclusively expressed in resting CD4+ T cells, is a new host antiviral factor targeted by Vpx. Other than Vpx from SIV mac and HIV-2, the Vpxrcm/nmd-2 lineage, which had no effect on the SAMHD1 protein, could strongly promote the degradation of KRT72, resulting in enhanced HIV-1 infection in resting CD4+ T cells. Furthermore, we discovered that KRT72 restricts HIV-1 replication by sequestering incoming HIV-1 capsids in cytoplasmic intermediate filaments (IFs). In the presence of KRT72, HIV-1 capsid cores become attached to the IF and their trafficking toward the nucleus is inhibited. In contrast, in the absence of KRT72, HIV-1 capsids are transported into the nucleus,leading to high levels of integrated HIV-1 DNA. In addition, KRT72 expression was substantially higher in resting CD4+ T cells than in activated CD4+ T cells, and it was rapidly reduced by T cell activation. Collectively, the results show that KRT72 is a new Vpx-counteracted host antiviral factor that acts to tether incoming capsids to the cytoplasmic IF, thereby restricting HIV-1 infection in resting CD4+ T cells.
