Project description:STAT3 is an immidiate regulator of Th17 differentiation. STAT3 difieciency downmodulate Th17 specific genes and Th17 responses. Therefore, we intend to identify genome wide targets of STAT3. We used microarrays to profile gene expression of STAT3 regulated genes during Th17 polarization. Total RNA was extracted from non-targeting and STAT3 siRNA treated Thp, Th0 and Th17 cell samples from different time points. Total RNA subjected to poly-A selection and hybridization on Affymetrix microarrays.
Project description:CD4+ T cells were extracted from mouse and human. They were activated in vitro with CD3/28 and cultured with Il4. ATAC-seq was then performed at different time points
Project description:Transcriptional analysis of human T cells differentiated in 4 T Helper context ( Th0, Th1, Th2 and Th17) in the presence or not of Interferon alpha We analyzed the transcriptomic profiles of 4 human naives T cells diferentiated in Th0, Th1, Th2 and Th17 in the presence or not of Interferon Alpha. Microarray analyses were performed in 2 time points : 1/ after Day 5 of polarization (= Day5); 2/ after Day 5+ four hours of re-stimulation (=Day 5+ 4H restim) in 3 different donors.
Project description:Microarray data on TH cell subsets from WT C57BL/6 and Bhlhe40 KO mice We used microarrays to detail the global programme of gene expression in polarized TH cell lineages Purified naïve CD4 T cells from spleen were polarized in vitro and then activated with PMA/Ionomycin prior to microarray analysis
Project description:To study the effect of Plasmodium falciparum-infected erythrocytes on gene expression in NK92 cells, microarray analysis after 6, 12 and 24 hours of co-culture with either uRBC or iRBC was performed. The aim was to identify pathways in NK92 cells that are switched on after iRBC encounter in a time-dependent manner that will help to understand the mechanisms in innate immune defenses against Plasmodium falciparum infection. Variation in gene expression of NK92 cells was determined after 6, 12, and 24 hours of co-culture with either infected or uninfected RBC compared to timepoint 0 (start of co-culture, untreated control). All experiments were done in triplicate, that means that samples were collected in 3 different experiments (A, B, and C) each time after 0, 6, 12 and 24 hours of co-culture.
Project description:The aim of this dataset was to study in detail the transcription kinetics initiated by cytokines IL-12 and IL-4 in early differentiation of Th1 and Th2 cells, respectively. Total RNA obtained from activated and IL-12 or IL-4 & anti-IL-12 treated cord blood CD4+ T cells, 12, 24, 48, and 72 hours after initiation of the cultures, compared to cells which were only activated. 37 samples were analyzed from three biological replicates of the culture. Several (26) of the Samples in this Series represent a re-analysis of CEL files originally submitted as GEO Series GSE17974. Please see associations on each Sample record.
Project description:The aim of this dataset was to study in detail the transcription kinetics initiated by cytokine IL-4 in early differentiation of Th2 cells. Total RNA obtained from activated and IL-4 & anti-IL-12 treated cord blood CD4+ T cells, 0.5, 1, 2, 4, 6, 12, 24, 48, and 72 hours after initiation of the cultures, compared to cells which were only activated. 57 samples were analyzed from three biological replicates of the culture. Two of the samples were discarded from the further data analysis due to compromised quality (samples 8=Th0.4h.1 and 11=Th2.6h.1).
Project description:Th1 and Th2 cells arise from a common precursor cell in response to triggering through the TCR and cytokine receptors for IL-12 or IL-4. This leads to activation of complex signaling pathways, which are not known in detail. Disturbances in the balance between type 1 and type 2 responses can lead to certain immune-mediated diseases. Thus, it is important to understand how Th1 and Th2 cells are generated. To clarify the mechanisms as to how IL-12 and IL-4 induce Th1 and Th2 differentiation and how TGF-beta can inhibit this process, we have used oligonucleotide arrays to examine the early polarization of Th1 and Th2 cells in the presence and absence of TGF-beta after 0, 2, 6 and 48 hours of polarization. Experiment Overall Design: This study includes altoghether 34 samples. Six different types of treatments (Thp, Th0, Th1, Th2, Th1+TGFbeta, Th2+TGFbeta) were studied at 4 time points (0, 2, 6 and 48h). There are two biological replicates, for both time series, consisting of pooled samples derived from different individuals. The early time points (0, 2 and 6h) and late time point (0 and 48h) were done in separate experiments (cell from different individuals), because of the limited number of the cells obtained from each the cord blood.
Project description:Uncontrolled Th17 cell activity is associated with cancer and autoimmune and inflammatory diseases. To validate the potential relevance of mouse models of targeting the Th17 pathway in human diseases we used RNA sequencing to compare the expression of coding and non-coding transcripts during the priming of Th17 cell differentiation in both human and mouse. In addition to already known targets, several transcripts not previously linked to Th17 cell polarization were found in both species. Moreover, a considerable number of human-specific long non-coding RNAs were identified that responded to cytokines stimulating Th17 cell differentiation. We integrated our transcriptomics data with known disease-associated polymorphisms and show that conserved regulation pinpoints genes that are relevant to Th17 cell-mediated human diseases and that can be modelled in mouse. Substantial differences observed in non-coding transcriptomes between the two species as well as increased overlap between Th17 cell-specific gene expression and disease-associated polymorphisms underline the need of parallel analysis of human and mouse models. Comprehensive analysis of genes regulated during Th17 cell priming and their classification to conserved and non-conserved between human and mouse facilitates translational research, pointing out which candidate targets identified in human are worth studying by using in vivo mouse models. Altogether 114 (57 human and 57 mouse) 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
Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to cytokine IL-4. Here we have analyzed on a genome wide level the STAT6 mediated gene expression after IL-4 induction in naive human CD4+ T cells. RNAi mediated STAT6 knockdown was used to reveal the genes specifically regulated by STAT6. Total RNA from STAT6 siRNA treated cord blood CD4+ T cells 12, 24, 48 or 72 hours after culturing the cells in activating (antiCD3+antiCD28) plus or minus IL-4 conditions was compared to total RNA from nonspecific control siRNA treated cells. All together 18 samples were analyzed and 3 biological replicates of the culture were performed for a total of 54 samples.