E-MTAB-5622
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5622 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-5622-analysis-methods.tsv | Tabular | |||
| E-MTAB-5622-analytics.tsv | Tabular | |||
| E-MTAB-5622-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-5622-configuration.xml | Xml | |||
| E-MTAB-5622-g1_g2-mvaPlot.png | Other |
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Project description:Transcriptional profiling of activated CD4+ memory T cells exposed to anti-TNF and recombinant human TNF-alpha in vitro
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Project description:We performed an RNA-seq analysis on FACS-sorted CD4+ memory T cells (Tmem, CD4+CD25-CD45RA-) stimulated in vitro with anti-CD3/CD28 coated beads (1:5), IL-2 (100 U/mL) in the presence of a TNF-alpha inhibitor (Etanercept, ETN, 5 μg/mL) or recombinant human TNF-alpha (rhTNF-alpha, 50 ng/mL) treatment. The cells were cultured for three days at 37°C and 5% CO2. On day three Tmem were lysed (Buffer RLT supplemented with DTT, QIAGEN) and RNA extraction was performed (RNeasy Plus Micro kit), followed by sample preparation with TruSeq (polyA) mRNA kits (Illumina), RNA sequencing (carried out by an Illumina HiSeq2500), and the alignment of trimmed fastQ files to GRCh38 human reference genome. We also performed a Quality control (QC). This was done using the tool FastQC FastQC/0.11.3-Java-1.7.0_80. QC metrics were calculated for the aligned reads using Picard-tools picard/1.130-Java-1.7.0_80, CollectRnaSeqMetrics, MarkDuplicates, CollectInsertSize-Metrics and SAMtools/1.2-foss-2015b flagstat. Finally, we carried out a Differential expression gene (DEG) analysis using DESeq2, in order to evaluate the impact of ETN and rhTNF-alpha on Transcriptome profiling of stimulated CD4+ Tmem. Principal Component Analysis (PCA) was carried out to visualise the samples given their entire transcriptome and any remaining batch effects.
2017-12-15 | E-MTAB-5622 | biostudies-arrayexpress
Project description:The experiment was designed to test how autocrine TNF-alpha impacts human CD4+ T cell activation. Naïve CD4+ T cells from healthy human blood donors were either left unactivated or activated with anti-CD3/anti-CD28 in presence of an isotype control antibody or anti-TNF-alpha antibody. RNA was extracter at 48 hours. Analysis revealed that anti-TNF-alpha treatment prevented upregulation of activation-induced T cell metabolic, signaling and effector molecules.
2024-07-25 | GSE238247 | GEO
Project description:CD4+ T-cells are key players in the pathogenesis of rheumatoid arthritis (RA) through potent production of inflammatory mediators including IL-17A, IFNg and TNF. Anti-TNF therapy has revolutionized the treatment of RA and we previously demonstrated that in vitro treatment of human CD4+ T-cells with the anti-TNF monoclonal antibody adalimumab (ADA) promotes anti-inflammatory IL-10 expression in multiple subpopulations of CD4+ T-cells. Here we investigated the transcriptional mechanisms underlying the IL-10 induction by TNF-blockade in in vitro stimulated CD4+ T-cells. CD4+ T-cells were isolated from PBMC of healthy volunteers by magnetic isolation and cultured for 3 days with anti-CD3/CD28 mAb in the absence or presence of anti-TNF. After culture, CD45RA+ cells were depleted and RNA was extracted for gene expression profiling by RNA-seq and cell nuclei were isolated for chromatin accessibility analysis by ATAC-seq. Gene expression analysis of memory CD4+ T-cells showed a distinct gene signature of 183 genes (q-value <0.05) conferred by anti-TNF treatment. Pathway enrichment analysis of the differentially expressed genes revealed multiple pathways related to cytokine signalling and regulation of cytokine production; in particular, IL10 was the most upregulated gene by anti-TNF, while the proinflammatory cytokines and chemokines IFNG, IL9, IL22 and CXCL10 were significantly downregulated (q-value <0.05). Transcription factor (TF) motif analysis at the differentially open chromatin regions after anti-TNF treatment revealed 58 TF motifs, shared by all donors, enriched at the IL10 locus. We identified 7 TF candidates for the anti-TNF mediated regulation of IL-10, which were either differentially expressed or whose locus was differentially accessible upon anti-TNF stimulation. We postulate that this TF network, which includes MAF and PRMD1, drives transcriptional regulation of IL-10 in anti-TNF treated T-cells.
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Project description:To examine the broad impact of IL-27 on human T lymphocytes, we performed a microarray analysis assessing >20,000 well annotated genes on purified naïve (CD45RA+CD45RO-CCR7+) and central memory (CD45RA-CD45RO+CCR7+) CD4+ and CD8+ T cells from three healthy donors that were activated in vitro (plate bound anti-CD3 and soluble anti-CD28) in the presence or absence of human recombinant IL-27 (100 ng/mL). Our goal was to investigate the impact of interleukin-27 on the gene expression profil of human CD4 and CD8 T lymphocytes.
2021-03-10 | GSE145334 | GEO
Project description:Effect anti-TNF-alpha treatment on CD4+ T cell activation
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Project description:Macrophages are heterogeneous immune cells with distinct origins, phenotypes, functions and tissue localization. Their susceptibility to HIV-1 is subject to variations from permissiveness to resistance, owing in part to regulatory microRNAs. Here, we used RNAseq to examine the expression of >400 microRNAs in productively infected and bystander cells of HIV-1-exposed macrophage cultures. Two micro-RNAs up regulated in bystander macrophages, miR-221 and miR-222, were identified as negative regulators of CD4 expression and CD4-mediated HIV-1 entry. Both microRNAs were enhanced by TNF-α, an inhibitor of CD4 expression. MiR-221/miR-222 inhibitors recovered HIV-1 entry in TNF-α-treated macrophages by enhancing CD4 expression, and increased HIV-1 replication and spread in macrophages by countering TNF-α-enhanced miR-221/miR-222 expression in bystander cells. In line with these findings, HIV-1-resistant intestinal myeloid cells express higher levels of miR-221 than peripheral blood monocytes. Thus, miR-221/miR-222 act as effectors of the antiviral host response activated during macrophage infection that restrict HIV-1 entry.
2017-09-11 | GSE103394 | GEO
Project description:Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis and premature cardiovascular death. Anti-TNF therapy is thought to reduce clinical cardiovascular disease risk and improve vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to explore the effects of certolizumab pegol (CZP) on TNF-activated human aortic endothelial cells (HAoECs. HAoECs were cultured in vitro and exposed to i) TNF alone, ii) TNF plus CZP, or iii) neither agent followed by transcription profiling.
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Project description:<p>We describe one patient with a heterozygous missense mutation in the coiled-coil domain of STAT5B. This patient presented with leukocytosis, lymphadenopathy, splenomegaly, necrotizing granulomas, hyper-IgM and autoimmune thrombocytopenia. Mutant STAT5B protein was shown to dominantly-interfere with IL2-induced transcriptional activity resulting in global downregulation of STAT5-regulated genes in patient T cells. The patient exhibited an increase in CD4+ T effector memory cells in the peripheral blood and these cells were resistant to restimulation-induced cell death <i>in vitro</i>. </p>
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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