Gene expression analysis in MZ twins discordant for IAR
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Fredrik Barrenas
PROVIDER: E-GEOD-37156 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Gene expression analysis in CD4+ T cells extracted from allergen-challenged PBMCs, isolated from discordant MZ twins with IAR MZ twins discordant for intermittent allergic rhinitis (IAR)
2012-04-14 | E-GEOD-37146 | biostudies-arrayexpress
Project description:Regulatory T (Treg) cells are involved in self tolerance, immune homeostasis, prevention of autoimmunity, and suppression of immunity to pathogens or tumours. The forkhead transcription factor FOXP3 is essential for Treg cell development and function as mutations in FOXP3 cause severe autoimmunity in mice and humans. However, the FOXP3-dependent molecular mechanisms leading to this severe phenotype are not well understood. Here we introduce the chromatin remodelling enzyme SATB1 (special AT-rich sequence-binding protein-1) as an important target gene of FOXP3. So far, SATB1 has been associated with normal thymic T-cell development, peripheral T-cell homeostasis, TH1/TH2 polarization, and reprogramming of gene expression. In natural and induced murine and human FOXP3+ Treg cells SATB1 expression is significantly reduced. While there is no differential epigenetic regulation of the SATB1 locus between Treg and Teffector cells, FOXP3 reduces SATB1 expression directly as a transcriptional repressor at the SATB1 locus and indirectly via miR-155 induction, which specifically binds to the 3’UTR of the SATB1 mRNA. Reduced SATB1 expression in FOXP3+ cells achieved either by overexpression or induction of FOXP3 is linked to significant reduction in TH1 and TH2 cytokines, while loss of FOXP3 function either by knock down or genetic mutation leads to significant upregulation of SATB1 and subsequent cytokine production. Alltogether, these findings demonstrate that reduced SATB1 expression in Treg cells is necessary for maintenance of a Treg-cell phenotype in vitro and in vivo and places SATB1-mediated T cell-specific modulation of global chromatin remodelling central during the decision process between effector and regulatory T-cell function. Gene expression profiling of freshly isolated CD4+ T cells, separated into CD25 negative and positive subpopulations, from three different donors. FOXP3 is stably and constitutively expressed at a high level in CD4+CD25+ regulatory T cells and at a low level in CD4+CD25- cells.
2011-08-13 | E-GEOD-15390 | biostudies-arrayexpress
Project description:The study aims at identifying transcriptional changes induced by in vitro polarization of human cord blood CD4+ cells towards Th17 subtype with combination of IL6, IL1b and TGFb by using timeseries data. In this study, we identified gene expression changes characterizing early stages of human Th17 cell differentiation program through genome-wide gene expression profiling. Primary T helper cells isolated from umbilical cord blood were used to construct detailed kinetic patterns of gene expression after initiation of Th17 differentiation with IL1b, IL6 and TGFb. The dataset described provides the starting point for defining the gene regulatory networks and identifying new candidates regulating the Th17 differentiation in human. Altogether 57 samples were analyzed representing 3 biological replicates of timeseries data (0, 0.5, 1, 2, 4, 6, 12, 24, 48 and 72 hours) of Th17 polarized cells and control Th0 cells
2012-05-03 | E-GEOD-35103 | biostudies-arrayexpress
Project description:Gene expression analysis in CD4+ T cells extracted from PBMCs, isolated from discordant MZ twins with IAR during season MZ twins discordant for intermittent allergic rhinitis (IAR)
2012-04-14 | E-GEOD-37155 | biostudies-arrayexpress
Project description:In order to identify genes expressed by cells that leave the spleen, the spleens were harvested from untreated reconstituted humanized mice (N=4) and a single cell suspension was prepared . The cultures were treated with either teplizumab (anti human CD3 hOKT3g1(Ala-Ala)) or hIg for 18 hrs in vitro. Splenocytes were also harvested 18 hrs after reconstituted mice (N=4) were treated with teplizumab in vivo. The humanized mice used where NOD/SCID IL2gc-/- (NSG) reconstituted with human CD34+ at birth. Total RNA was obtained form sorted human CD4 splenocytes 18 hours post treatment. Comparsons were made between the treatment groups.
2012-02-27 | E-GEOD-34163 | biostudies-arrayexpress
Project description:Analysis of transcriptional differences between aberrant (surface CD3-) RCDII cell lines and regular (surface CD3+) intraepithelial cell lines in order to characterize aberrant RCDII cells. All cell lines were cultured from duodenal biopsies of RCDII or non-RCDII (either celiac or non-celiac) patients. We compared 3 RCDII cell lines from RCDII patients P1-P3 with the following control cell lines: CD3+CD4+ T cell line from P1 and P3, CD3+CD8+ T cell line from P3 and mixed CD4/CD8+ T cell lines from non-RCDII patients. All control cells matched the phenotype of mature T cells (CD3+CD4+ and/or CD3+CD8+). Samples were randomly distributed among two BeadChips and measured in duplicates.
2012-06-11 | E-GEOD-33078 | biostudies-arrayexpress
Project description:We screened the differential expressed microRNA from the rheumatoid arthritis patients and healthy person in their hydrops articuli CD4+ T cells. We screened the differential expressed microRNA from the rheumatoid arthritis patients and healthy person in their hydrops articuli CD4+ T cells. 1.Isolated the CD4+ T cells from the hydrops articuli cells of 2 rheumatoid arthritis patients. 2.Isolated the CD4+ T cells from healthy person's peripheral blood as control. 3.Isolation of total RNA from CD4+ T cells then sent the samples to KangChen Bio-tech Inc (Shanghai, China) where they were labeled, hybridized, scaned, normalied and transformed to the final data.
2010-04-03 | E-GEOD-21118 | biostudies-arrayexpress
Project description:Effective immune responses depend upon appropriate T cell differentiation in accord with the nature of an infectious agent, and the contingency of differentiation depends minimally on T cell antigen receptor, co-receptor, and cytokine signals. In this reverse genetic study we show that the Map Kinase, Erk2, is nonessential for T cell proliferation in the presence of optimum co-stimulation. Instead, it has opposite polar effects on T-bet and Gata3 expression and hence on Th1 and Th2 differentiation. Alternatively, in the presence of TGFbeta, the Erk pathway suppresses a large program of gene expression effectively limiting the differentiation of Foxp3+ T reg cells. In the latter case, the mechanisms involved include suppression of Gata3 and Foxp3, induction of Tbx21, phosphorylation of Smad2,3, and possibly suppression of Socs2, a positive inducer of Stat5 signaling. Consequently, loss of Erk2 severely impeded Th1 differentiation while enhancing the development of Foxp3+ induced T regulatory cells. Selected profiles of gene expression under multiple conditions of T cell activation illustrate the opposing consequences of Erk pathway signaling. Analysis of the Th1 and iTreg differentiation regulated by Erk2. Total RNA obtained from WT or Erk2 deficient CD4 T cells in different conditions.
2012-06-30 | E-GEOD-37554 | biostudies-arrayexpress
Project description:Background: Development of target specific therapeutics greatly benefits from simultaneous identification of biomarkers to determine aspects of bioactivity, drug safety and efficacy or even treatment outcome. This is particularly important when targeting pleiotropic factors such as the TGFbeta system. TGFbeta has become a prime target for cancer therapeutics since inhibition of TGFbeta signaling simultaneously attacks the tumor and its microenvironment. Methods: Here we introduce blood transcriptomics followed by a defined set of validation assays as a promising approach to identify novel biomarkers for monitoring TGFbeta therapy. Findings: Our initial genome-wide analysis of transcription in peripheral blood revealed 12 candidate genes specifically regulated in peripheral blood by the TGFbeta receptor I kinase inhibitor LY2109761. In subsequent in vitro and in vivo molecular and immunological analyses, the combined monitoring of gene regulation of three genes, namely TMEPAI, OCIAD2, and SMAD7 was established as novel biomarkers for anti-TGFbeta based therapies. Interpretation: Overall, the proposed algorithm of biomarker identification is easily adapted towards other drug candidates for which gene regulation can be established in peripheral blood. CD4+ T cells were serum-deprived for 12 hours followed by 8 hours incubation with the indicated compounds, total of 22 samples.
2010-07-20 | E-GEOD-15468 | biostudies-arrayexpress
Project description:Generation of effective immune responses requires expansion of rare antigen-specific CD4+ T cells. The magnitude of the response is ultimately determined by proliferation and survival. Both processes are tightly controlled to limit responses to innocuous antigens. Sustained expansion occurs only when innate immune sensors are activated by microbial stimuli or by adjuvants, which has important implications for vaccination. The molecular identity of the signals controlling sustained T cell responses is not fully clear. Here we describe a prominent role for the Notch pathway in this process. Co-activation of Notch allows accumulation of far greater numbers of activated CD4+ T cells than stimulation via T cell receptor and classical co-stimulation alone. Notch does not overtly affect cell cycle entry or progression of CD4+ T cells. Instead, Notch protects activated CD4+ T cells against apoptosis after an initial phase of clonal expansion. Notch induces a broad anti-apoptotic gene expression program, which protects against intrinsic as well as extrinsic apoptosis pathways. Both Notch1 and Notch2 receptors and the canonical effector RBPJ are involved in this process. Correspondingly, CD4+ T cell responses to immunization with protein antigen are strongly reduced in mice lacking these components of the Notch pathway. Our findings therefore show that Notch controls the magnitude of CD4+ T cell responses by promoting cellular longevity. Naïve CD4+ T cells were activated for 1 day (1 control sample and 1 experimental sample) or 3 days (3 control samples and 3 experimental samples) with antibodies to CD3 soluble and CD28 in the presence of recombinant Delta4-Ig (experimental samples) or control Ig (control samples).
2012-02-04 | E-GEOD-35547 | biostudies-arrayexpress