Similar Datasets
Project description:Exosomes were isolated from CD4+T cell by ExoQuickTC kit in rheumatoid arthritis patients and controls. Proteomic analysis of CD4+ T-cell-derived exosomes was performed by TMT combined with LC‒MS/MS.
2023-06-30 | PXD043469 |
Project description:Functionally distinct CD4+ helper T (Th) cell subsets, such as Th1, Th2, Th17, and regulatory T cells (Treg), play a pivotal role in the host-defense against pathogen invasion and the pathogenesis of inflammatory disorders. In this project, DIA-MS-based proteome analysis was performed on naïve CD4+ T, Th0, Th1, Th2, Th17 and iTreg cells using Q Exactive HF-X (Thermo Fisher Scientific) to search for proteins that differ among the cell subsets.
2023-01-04 | PXD036065 | JPOST Repository
Project description:CD4 T cell transcriptome and RARα
| PRJNA832807 | ENA
Project description:Naive CD4+ T cell activation transcriptome
| PRJNA171178 | ENA
Project description:To mount an anti-pathogen response, CD4 T cells must undergo rapid cell proliferation. However, poorly controlled expansion can result in diseases such as autoimmunity. One important regulator of T cell activity is the E3 ubiquitin ligase Itch. Itch deficient patients suffer from extensive autoinflammation. Similarly, Itch deficient mice exhibit inflammation characterized by high numbers of activated CD4 T cells. While the role of Itch in limiting CD4 T cell cytokine production has been extensively studied, it is less clear whether and how Itch regulates proliferation of these cells. We determined that Itch deficient CD4 T cells are hyperproliferative in vitro and in vivo, due to increased S phase entry. Whole cell proteomics analysis of Itch deficient primary mouse CD4 T cells revealed increased abundance of the -catenin co-activator WW domain binding protein 2 (WBP2). Furthermore, Itch deficient cells demonstrate increased WBP2 protein stability, and Itch and WBP2 interact in CD4 T cells. Knockdown of WBP2 in CD4 T cells caused reduced proliferation. Together, our data support that Itch attenuates CD4 T cell proliferation by promoting WBP2 degradation. This study identifies novel roles for Itch and WBP2 in regulating CD4 T cell proliferation, providing insight into how Itch may prevent inflammation.
2021-01-07 | PXD019272 | Pride
Project description:We compared the methylated and non-methylated regions in the genome of ex vivo-isolated naive CD4+ T cells, Th1 cells, Th17 cells and regulatory T cells by methyl-CpG binding domain protein sequencing (MBD-seq). Naive T cells and Th1 cells share more methylated regions than naive T cells and Th17 cells or Th1 and Th17 cells. However, analysis of the non-methylated regions revealed the highest similarity between Th1 and Th17 cells. Another aim was the analysis of the Th17 lineage on the basis of the methylome. We searched for regions absent in the methylome of Th17 but present in naive T cells, Th1 cells and regulatory T cells. Here, we identified differential methylation in the loci of Il17a, Chn2, Dpp4 and Dclk1. CD4+ T effector cells were prepared ex vivo, stimulated with PMA/Ionomycin, subjected to a comercially available cytokine secretion kit (IL-17A and IFNg), stained by adding fluorescence-labeled antibodies against CD3, CD4 and CD45RB and sorted by flow cytometry. We sorted naive CD4+ T cells (CD3+CD4+CD45RB_high), Th1 cells (CD3+CD4+CD45RB_low_IFNg+IL17A-), Th17 cells (CD3+CD4+CD45RB_low_IFNg-IL17A+) and regulatory T cells (CD3+CD4+CD25++).
2013-12-31 | E-GEOD-45911 | biostudies-arrayexpress
Project description:Upon antigen-specific T Cell Receptor (TCR) engagement, human CD4+ T cells proliferate and differentiate, a process associated with rapid transcriptional changes and metabolic reprogramming utilizing aerobic glycolysis together with maintenance of oxidative phosphorylation1,2. However, the role of glycolytic-reprogramming during T-cell activation remains largely unclear3,4,5. Here, we show that maintenance of cytosolic pyruvate production is an essential requirement for remodeling of the CD4+ T cell epigenome after TCR-engagement. Furthermore, we provide evidence that the local inflammatory environment sustains metabolic reprogramming of CD4+ T-cells and impacts histone modification in a pyruvate-dependent manner. Mechanistically, we demonstrate that rapid and sustained generation of cytosolic, but not mitochondrial, pyruvate is an essential step for acetyl-coA production and subsequent H3K27ac epigenome remodeling. TCR-activation was found to induce nuclear import of pyruvate dehydrogenase (PDH) and its association with both the p300 acetyltransferase and histone H3K27ac. Disrupting PDH nuclear import impacted expression of activation-induced genes. These results reveal a direct connection between CD4+ T cell metabolic reprogramming and transcriptional regulation, with the generation of cytosolic pyruvate being an essential step in T cell activation. These data support tight integration of metabolic enzymes and histone modifying enzymes, allowing metabolic reprogramming to fuel CD4+ T cell activation.
2023-10-27 | PXD018132 | Pride
Project description:<p>We use next generation sequencing to investigate the different transcriptomes of closely related CD4+ T-cells from healthy human donors to elucidate the genetic programs that underlie their specialized immune functions. Six cell types were included: Regulatory T-cells (CD25hiCD127low/neg with >95% FOXP3+ purity), regulatory T-cells activated using PMA/ionomycin, CD25-CD45RA+ ('naive' helper T-cells), CD25-CD45RO+ ('memory' helper T-cells), activated Th17 cells (>98% IL17A+ purity) and activated IL17-CD4+ T-cells (called 'ThPI'). Poly-T capture beads were used to isolate mRNA from total RNA, and fragment sizes of ~200 were sequenced from both ends on Illumina's genome analyzer. We confirm many of the canonical signature genes of T-cell populations, but also discover new genes whose expression is limited to specific CD4 T-cell lineages, including long non-coding RNAs. Additionally, we find that genes encoded at loci linked to multiple human autoimmune diseases are enriched for preferential expression upon T-cell activation, suggesting that an aberrant response to T-cell activation is fundamental to pathogenesis.</p>
| phs000626 | dbGaP
Project description:We previously found that NF-kB inducing kinase (NIK) overexpression in T cells via CD4 promoter driven transgene induction caused lethal autoimmunity in mice. Autoimmunity was associated with increased conventional T cell effector function and decreased regulatory T cell (Foxp3+CD4+) suppression. The goal in this study was to elucidate global transcriptional changes in Foxp3+CD4+ and Foxp3-CD4+ T cells intrinsically caused by chronic NIK overexpression in these cell types. Total RNA from FACS-sorted NIKtg and WT Foxp3RFP+CD4+ and Foxp3RFP-CD4+ harvested from NIKtg/CD4Cre/Foxp3RFP + WT/Thy1.1/Foxp3RFP mixed bone marrow chimeric mice, >8 weeks after bone marrow reconstitution.
2016-04-29 | GSE80756 | GEO