Project description:The aim of this study was to determine whether asthma with depression is characterized by unique pathophysiological pathways by analyzing the global gene expression patterns of CD4+ lymphocytes from asthmatics with or without depression.
Project description:Analysis of expression quantitative trait loci (eQTLs) using RNA derived from freshly harvested peripheral blood CD4+ lymphocytes from 200 asthmatics collected in clinical settings.
Project description:Analysis of expression quantitative trait loci (eQTLs) using RNA derived from freshly harvested peripheral blood CD4+ lymphocytes from 200 asthmatics collected in clinical settings. RNA was obtained from peripheral blood CD4+ lymphocytes at four study centers. Peripheral blood (17 cc) was collected into BD Vacutainer CPT tubes (BD Diagnostics, Franklin Lakes, New Jersey) and placed on ice. Samples were centrifuged within 1 hour of collection for 20 minutes at 1700RCF, followed by mononuclear cell layer isolation and suspension in 10 ml of PBS. We isolated CD4+ lymphocytes using anti-CD4+ microbeads by column separation (Miltenyi Biotec, Auburn, CA) using 20 µl anti-CD4+ Micro beads per 106 total cells
Project description:Reveal differentially regulated genes and cellular pathways within allergic and non-allergic asthmatic children compared to healthy controls Peripheral blood mononuclear cells (PBMCs) were obtained from allergic asthmatics (n=14), non-allergic asthmatics (n=8) and healthy controls (n=14) and kept with anti-CD3/CD28 (CD328), LpA or without stimulation (M).
Project description:To investigate the effect of nicotinamide mononucleotide (NMN) on CD4+ T cells, primary human CD4+ T cells purified from peripheral blood mononuclear cells of healthy donors were treated without or with NMN. Expression profiling analysis on either host gene or viral gene was performed using data obtained from bulk RNA-seq of NMN-treated and untreated (control) CD4+ T cells at 48 hours post treatment and/or post infection.
Project description:Single cell transcriptomic analysis of human CD25+ CD127- CD4+ Treg cells and CD25- CD127+ CD4+ Tconv cells isolated from peripheral blood from two different donors
Project description:Background: Functional enrichment analysis of genome-wide association study (GWAS)-summary statistics has suggested that immune cell-types, and especially CD4+ T-cells, play an important role in asthma pathogenesis. Despite this, CD4+ T-cells are under-represented in asthma transcriptome studies. Objective: To identify differences in gene expression between asthmatics and healthy controls in CD4+ T-cells. Methods: CD4+ T-cells were isolated within 2 hours from collection from peripheral blood from people with well-established asthma (n=33) and healthy controls (n=12). 3'-RNA-Seq was used to generate gene expression data. Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify sets of co-expressed genes (modules). The asthma-associated modules were tested for enrichment of GWAS-identified asthma genes and gene ontology (GO) biological processes. For the genes in the asthma-associated modules, integration of eQTL and GWAS summary statistics (colocalisation), and protein-protein interaction (PPI) data was used to identify master regulators. Results: After quality control, 43 samples were available for the analysis. WGCNA identified three modules associated with asthma, which are strongly enriched for GWAS-identified asthma genes, antigen processing/presentation and immune response to viral infections. Colocalisation analysis of eQTL and GWAS summary statistics, together with PPI data, identified PTPRC as a master regulator of asthma gene-expression profiles in CD4+ T-cells. Conclusion: Unstimulated CD4+ T-cells from peripheral blood from asthmatics have different expression profiles, compared to healthy controls, for sets of genes involved in immune response to viral infections and antigen processing/presentation . Integration of genetic and protein-protein interaction data identified PTPRC as a master regulator of genes in asthma.
