Similar Datasets
Project description:RNA expression in CCL19-treated CD4+ T cells
| PRJNA923181 | ENA
Project description:Naïve CD4+ T cells were purified from the spleens using the EasySep Mouse Naïve CD4+ T Cell Isolation Kit (STEMCELL Technologies). The purified T cells were stimulated with plate-bound anti-CD3 (1 μg /ml) and anti-CD28 (2 μg/ ml) antibodies in replicate wells of 96-well plates.
| PXD062495 |
Project description:Approximately 10% to 20% of patients optimally treated for early Lyme disease develop persistent symptoms of unknown pathophysiology termed posttreatment Lyme disease syndrome (PTLDS). The objective of this study was to investigate associations between PTLDS and immune mediator levels during acute illness and at several time points following treatment. Seventy-six participants with physician-documented erythema migrans and 26 healthy controls with no history of Lyme disease were enrolled. Sixty-four cytokines, chemokines, and inflammatory markers were measured at each visit for a total of 6 visits over 1 year. An operationalized definition of PTLDS incorporating symptoms and functional impact was applied at 6 months and 1 year following treatment completion, and clinical outcome groups were defined as the return-to-health, symptoms-only, and PTLDS groups. Significance analysis of microarrays identified 7 of the 64 immune mediators to be differentially regulated by group. Generalized logit regressions controlling for potential confounders identified posttreatment levels of the T-cell chemokine CCL19 to be independently associated with clinical outcome group. Receiver operating characteristic analysis identified a CCL19 cutoff of >111.67 pg/ml at 1 month following treatment completion to be 82% sensitive and 83% specific for later PTLDS. We speculate that persistently elevated CCL19 levels among participants with PTLDS may reflect ongoing, immune-driven reactions at sites distal to secondary lymphoid tissue. Our findings suggest the relevance of CCL19 both during acute infection and as an immunologic risk factor for PTLDS during the posttreatment phase. Identification of a potential biomarker predictor for PTLDS provides the opportunity to better understand its pathophysiology and to develop early interventions in the context of appropriate and specific clinical information.
2016-07-20 | GSE84479 | GEO
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.
2010-01-09 | E-GEOD-18524 | biostudies-arrayexpress
Project description:Technological advances in genomics, epigenomics, transcriptomics and proteomics have enabled massively parallel measurements across thousands of genes and gene products. Such high-throughput technologies have been extensively used to carry out genome-wide studies particularly in the context of diseases. Nevertheless, a unified analysis of the genome, epigenome, transcriptome, and proteome of a single mammalian cell type to obtain a coherent view of the complex interplay between omes has not yet been undertaken. Here, we report the first multi-omic analysis of human primary naïve CD4+ T cells, revealing hundreds of unannotated mRNA transcripts, miRNAs, pseudogenes, and noncoding RNAs. Additionally, we carried out a comparative analysis of naïve CD4+ T cells with primary resting memory CD4+ T cells, which have provided novel insights into T cell biology. Overall, our data will serve as a baseline reference of a single pure population of cells for future systems level analysis of other defined cell populations.
2015-11-12 | PXD000376 | Pride
Project description:We compared differences in fetal and adult T cells by performing whole genome profiling on sort-purified T cells (naïve CD4+ and Treg cells) from human fetal specimens (18-22 gestational weeks) and adult specimens (age 25-40 years old). Fetal and Adult Naïve CD4+ T cells phenotype: CD3+CD4+CD45RA+CCR7+CD27+, Fetal and Adult CD4+CD25+ Treg phenotype: CD3+CD4+CD25bright Four different groups were analyzed: Fetal Naïve CD4+ T cells, Adult Naïve CD4+ T cells, Fetal Treg cells, Adult Treg cells. For each group three independent donors were analyzed.
2010-12-17 | E-GEOD-25087 | biostudies-arrayexpress
Project description:Objective. TNF? is a potent pro-inflammatory cytokine playing a pivotal role in several autoimmune diseases. Neutralizing TNF? inhibits T cell proliferation and IFN? production, and enhances suppressive capacity of regulatory T cells (Treg). Little is known about the mechanism of TNF? blocking agents on naïve T cell differentiation. Methods. Naïve CD4+ T cells were activated by dendritic cells (DC) in presence or absence of anti-TNF? agents. T cell polarization and activation was assessed during T cell differentiation. In addition, whole genome gene expression analysis was performed on anti-TNF?-treated T cells. Results. Neutralizing TNF? during priming of naïve CD4+ T cells by DC favors development of IL-10+ T helper (Th) cells at the expense of IFN? induction. TNF? inhibits IL-10 via TNFRII, which becomes expressed after naïve T cell activation. While initial CD4+ T cell activation was not affected, neutralization of TNF? negatively affected later stages of T cell priming by counteracting full T cell activation and survival. Whole genome gene expression analysis revealed a regulatory gene profile of anti-TNF?-treated T cells. Indeed, neutralizing TNF? during naïve T cell priming enhanced the suppressive function of anti-TNF?-treated T cells. Conclusion. Inhibition of TNF?–TNFRII interaction affects late stage effector T cell development and shifts the balance of Th cell differentiation towards IL-10 expressing regulatory T cells, which may be one of the beneficial mechanisms in TNF? blocking therapies. Naïve CD4+ T cells were CFSE labeled and co-cultured for 13 days with allogeneic dendritic cells in the presence or absence of anti-TNF? agents. After 13 days, the CFSElow T cells were FACS sorted. Samples were generated from three independent donors.
2014-06-25 | E-GEOD-42812 | biostudies-arrayexpress
Project description:Differences in DNA methylation have been reported in B and T lymphocyte populations, including CD4+ T cells, isolated from rheumatoid arthritis (RA) patients when compared to healthy controls. CD4+ T cells are a heterogeneous cell type with subpopulations displaying distinct DNA methylation patterns. In this study, we investigated DNA methylation using reduced representation bisulfite sequencing in two CD4+ T cell populations (CD4+ memory and naïve cells) in three groups: newly diagnosed, disease modifying antirheumatic drugs (DMARD) naïve RA patients (N=11), methotrexate (MTX) treated RA patients (N=18), and healthy controls (N=9) matched for age, gender and smoking status. Analyses of these data revealed significantly more differentially methylated positions (DMPs) in CD4+ memory than in CD4+ naïve T cells (904 vs 19 DMPs) in RA patients compared to controls. The majority of DMPs (72%) identified in newly diagnosed and DMARD naïve RA patients with active disease showed increased DNA methylation (39 DMPs), whereas most DMPs (80%) identified in the MTX treated RA patients in remission displayed decreased DNA methylation (694 DMPs). Interestingly, we also found that about one third of the 101 known RA risk loci overlapped (+/- 500 kb) with the DMPs. Notably, introns of the UBASH3A gene harbour both the lead RA risk SNP and two DMPs in CD4+ memory T cells. Our results suggest that RA associated DNA methylation differences vary between the two T cell subsets, but are also influenced by RA characteristics such as disease activity, disease duration and/or MTX treatment.
2020-02-07 | GSE135770 | GEO
Project description:(1) Transcriptional profiling of mouse CD4 T cells comparing naïve HY-specific TCR transgenic T cells with the same cells recovered after adoptive transfer into WT female C57BL/6 mice on day 5 following treatment with HY peptide (100microgrammes intranasally days 1,2 and 3) and comparing naïve HY-specific TCR transgenic T cells with the same cells recovered after adoptive transfer into WT female C57BL/6 mice on day 5 following treatment with HY peptide plus LPS (100microgrammes peptide and 20microgrammes LPS intranasally day 1) (2)Transcriptional profiling of mouse CD8 T cells comparing naïve CD8 T cells with HY-tetramer positive cells recovered from tolerant peptide treated (see above) WT female C57BL/6 mice on day 22 after male skin graft or 10-15 days after treatment with male spleen cells and comparing naïve CD8 T cells with HY-tetramer positive cells recovered from untreated (rejecting) WT female C57BL/6 mice on day 22 after male skin graft or 10-15 days after treatment with male spleen cells.
2011-03-28 | GSE26908 | GEO
Project description:We investigated the role of CMTR1 in T cells using an Cmtr1 conditional knockout mouse model. We report that the cap-specific RNA (nucleoside-2'-O-)-methyltransferase, CMTR1, supports naïve T cell survival and activation-induced proliferation. We demonstrate that CMTR1 has gene-specific impacts in T cells. These RNAseq experiments investigate the effect of Cmtr1 cKO on the naïve CD4 T cell transcriptome.
2025-10-16 | GSE198474 | GEO