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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Epigenomic analysis of primary human T cells reveals novel enhancers associated with Th2 memory differentiation and asthma susceptibility (3 cell types)

ABSTRACT: A characteristic feature of asthma is the aberrant accumulation, differentiation or function of memory CD4+ T cells that produce Th2 cytokines (Th2 cells). By mapping genome-wide histone modification profiles of T cell subsets isolated from peripheral blood of healthy and asthmatic individuals, we identified enhancers with known and potential roles in the normal differentiation of human Th1 and Th2 cells. In addition, we discovered disease-specific T cell enhancers that differ between healthy and asthmatic individuals. Examination of H3K4me2 histone modifications in 3 human cell types in 11 healthy and 12 asthmatic individuals .

ORGANISM(S): Homo sapiens

SUBMITTER: Anna Gerasimova

PROVIDER: E-GEOD-53643 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression (RNA-Seq) analysis of primary human T cells reveals novel genes associated with Th2 memory differentiation and asthma susceptibility

Project description:A characteristic feature of asthma is the aberrant accumulation, differentiation or function of memory CD4+ T cells that produce Th2 cytokines (Th2 cells). By comparing gene expression profiles of T cell subsets isolated from peripheral blood of healthy and asthmatic individuals, we identified genes with known and potential roles in the normal differentiation of human Th1 and Th2 cells. Examination of gene expression in 3 human cell types in healthy and asthmatic individuals.

2014-07-05 | E-GEOD-55320 | biostudies-arrayexpress

Reproducibility of standard and micro-scaled H3K4me2 ChIP-Seq assay in mouse derived lymphoblastic cell line (D10.G4.1 cells, ATCC)

Project description:To estimate the reproducibility of standard and micro-scaled H3K4me2 ChIP-Seq assay we performed the genome-wide correlation analysis of H3K4me2 enrichment patterns from 7 independent standard ChIP-Seq assays (2 million D10 cells), and micro-scaled ChIP-Seq 100,000 cells sample M-bM-^@M-^S(N=12), 10,000 cells sampleM-bM-^@M-^S(N=3), and 1000 cell sample M-bM-^@M-^S (N=4) Examination of H3K4me2 histone modifications in mouse derived lymphoblastic cell line (D10.G4.1 cells, ATCC).

2014-07-05 | E-GEOD-53644 | biostudies-arrayexpress

A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice

2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress

Defining a Th9 transcriptome

Project description:Microarray analyses were performed to compare gene expression in cultured mouse Th9, Th2 and Treg cells and resting versus activated Th9 cells. Three replicates were analyzed for each culture condition; Th9 unstim, Th2 unstim, Treg unstim, Th9 stim

2014-03-26 | E-GEOD-44937 | biostudies-arrayexpress

Epigenomic analysis of primary human T cells reveals novel enhancers associated with Th2 memory differentiation and asthma susceptibility (3 cell types)

Project description:A characteristic feature of asthma is the aberrant accumulation, differentiation or function of memory CD4+ T cells that produce Th2 cytokines (Th2 cells). By mapping genome-wide histone modification profiles of T cell subsets isolated from peripheral blood of healthy and asthmatic individuals, we identified enhancers with known and potential roles in the normal differentiation of human Th1 and Th2 cells. In addition, we discovered disease-specific T cell enhancers that differ between healthy and asthmatic individuals.

2014-07-05 | GSE53643 | GEO

Epigenomic analysis of primary human T cells reveals novel enhancers associated with Th2 memory differentiation and asthma susceptibility

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-07-05 | E-GEOD-53646 | biostudies-arrayexpress

Differential gene expression of lymphocytes stimulated with rhinovirus species A and C in asthmatic and non-asthmatic children

Project description:Background: Evidence suggests that immune responses to rhinovirus A and C are altered in asthmatic children and rhinovirus species induce different types of antibody responses. Objective: To ascertain and compare the T-cell memory response induced by RV-A and RV-C in asthmatic and non-asthmatic children. Methods: Peripheral blood mononuclear cells from children who previously suffered asthma exacerbation (asthmatics) and non-asthmatic controls were stimulated in vitro with peptide formulations to induce representative species-specific responses to RV-A and RV-C. Expression of genes was measured by RNA-seq and differentially expressed genes were further analysed to identify enriched pathways and upstream regulators. Results: Responses to RV-A showed markedly higher upregulation of IFNG and the IFNG responsive genes CXCL9, 10 and 11 and STAT1 compared to RV-C. There was no reciprocal upregulation of Th2 cytokine genes or the Th2 chemokine genes CCL11, CCL17 and CCL22. RV-C but not RV-A induced high upregulation of CCL24 (eotaxin-2) in both non-asthmatic and asthmatic responses. Upstream regulator analysis showed both RV-A and, although to a diminished extent, RV-C induced predominant Th1 and inflammatory cytokine expression. The responses of asthmatics compared to non-asthmatics was diminished to both RV-A and RV-C while retaining the pattern for gene expression and upstream regulators characteristic of each species and there was no upregulation of Th2-type responses. All groups showed activation of the IL-17A pathway. Conclusions: RV-C induced memory cells with a lower IFNG type response than RV-A without Th2 upregulation. Asthmatics had lower recall responses than non-asthmatics while largely retaining the same gene activation profile for each species.

2020-08-10 | GSE135192 | GEO

Gene expression (RNA-Seq) analysis of primary human T cells reveals novel genes associated with Th2 memory differentiation and asthma susceptibility

2014-07-05 | GSE55320 | GEO

Expression and regulation of lincRNAs during T cell development and differentiation

Project description:Although lincRNAs are implicated in regulating gene expression in various tissues, little is known about lincRNA transcriptomes in the T cell lineages. Here we identify 1,524 lincRNAs in 42 T cell samples from early T cell progenitors to terminally differentiated T helper subsets. Our analysis revealed highly dynamic and cell-specific expression patterns of lincRNAs during T cell differentiation. Importantly, these lincRNAs are located in genomic regions enriched for protein-coding genes with immune-regulatory functions. Many of these transcripts are bound and regulated by the key T cell transcription factors, T-bet, GATA3, STAT4 and STAT6. We demonstrate that the lincRNA LincR-Ccr2-5'AS, together with GATA3, is an essential component of a regulatory circuit in Th2-specific gene expression. To obtain comprehensive profiles of lincRNA expression during the development and differentiation of T cell lineages, we purified CD4-CD8 double negative (DN) cells (DN1, DN2, DN3 and DN4), double positive (DP) cells (CD4+CD8+CD3low and CD4+CD8intCD69+), single positive (SP) CD4 and CD8 cells, and thymic-derived regulatory T cells (tTreg) from thymi of C57BL/6 mice. Additionally, we obtained Th1, Th2, Th17 and iTreg cells by in vitro differentiation of naM-CM-/ve CD4 T cells for a various length of time in culture (4 hrs, 8 hrs, 12 hrs, 24 hrs, 48 hrs, 72 hrs, 1 week, 2weeks). Total and/or polyadenylated RNAs from these cells was analyzed using RNA-Seq. To understand the regulation of lincRNAs by T cell master regulator T-bet, we compared the transcriptiomes between T-bet deficient Th1 cells and control Th1 cells. We did similar experiments and data analysis for STAT4 (Th1), GATA3 (Th2) and STAT6 (Th2). Finally, to address the funcation of a Th2-specifically expressed lincRNA, lincR-Ccr2-5'AS, we compared the transcriptomes between lincR-Ccr2-5'AS knockdown Th2 cells and control Th2 cells.

2013-09-23 | E-GEOD-48138 | biostudies-arrayexpress

Cytokine receptor modulation by interleukin-2 broadly regulates T helper cell lineage differentiation

Project description:T helper (Th) cells control host defense to pathogens. IL 12R expression is required for Th1, IL-4RM-NM-1 for Th2, and IL-6RM-NM-1/gp130 for Th17 differentiation to allow responsiveness to IL-12, IL-4, and IL-6, respectively. IL-2 via STAT5 controls Th2 differentiation by regulating the Th2 cytokine gene cluster and Il4ra expression. Here we show that IL-2 regulates Th1 differentiation, inducing STAT5-dependent IL-12RM-NM-22 and T-bet expression, with impaired human Th1 differentiation when IL-2 was blocked. Th1 differentiation was also impaired in mouse Il2-/- T cells but restored by IL-12RM-NM-22 expression. Consistent with IL-2M-bM-^@M-^Ys inhibition of Th17 differentiation, IL-2 decreased Il6ra and Il6st/gp130 expression, and Il6st augmented Th17 differentiation even when IL-2 was present. Thus, IL-2 influences T-cell differentiation by modulating cytokine receptor expression to help specify/maintain differentiated states. Genome-wide mapping of STAT1,STAT4,STAT5A,STAT5B binding to their target genes in Th1 or human CD4+ cells was conducted

2011-04-24 | E-GEOD-27158 | biostudies-arrayexpress

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