Similar Datasets
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: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.
2012-05-04 | GSE35103 | GEO
Project description:Using an unbiased chemical biology approach, we discover harmine as a novel regulator of Treg/Th17 differentiation. Harmine enhances Treg differentiation (working in conjunction with low levels of exogenous TGFb) and inhibits Th17 differentiation. Analysis of global gene expression of Tregs generated using low TGFb + harmine reveals significant similarity to Tregs generated using high TGFb only and suggests relevance of harmine-engaged mechanisms to IBD. Naïve CD4+CD62L+ T cells were purified from Foxp3GFP mice either by MACS or FACS, then cultured in either low TGFb + harmine or high TGFb conditions. GFP+ Tregs were sorted by FACS at day 4.
2015-04-29 | E-GEOD-64247 | biostudies-arrayexpress
Project description:Transcriptome analysis of TLR2-activated Th17 cells
| PRJNA730008 | ENA
Project description:CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity1-4. Crucial for T helper17 (Th17) cells in vivo5,6, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification7-10. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. Neither IL-6 nor IL-23 alone efficiently generated Th17 cells; however, these cytokines in combination with IL-1β effectively induced IL-17 production in naïve precursors, independently of TGF-β. Epigenetic modification of the Il17a/Il17f and Rorc promoters proceeded without TGF-β1, allowing the generation of cells that co-expressed Rorγt and T-bet. T-bet+Rorγt+ Th17 cells are generated in vivo during experimental allergic encephalomyelitis (EAE), and adoptively transferred Th17 cells generated with IL-23 in the absence of TGF-β1 were more pathogenic in this experimental disease. These data suggest a new model for Th17 differentiation. Consistent with genetic data linking the IL23R with autoimmunity, our findings re-emphasize the role of IL-23 and therefore have important implications for the development of new therapies. Mouse T helper 17 cell differentiation with or without TGFB
2010-08-31 | E-GEOD-23505 | biostudies-arrayexpress
Project description:Using an unbiased chemical biology approach, we discover harmine as a novel regulator of Treg/Th17 differentiation. Harmine enhances Treg differentiation (working in conjunction with low levels of exogenous TGFb) and inhibits Th17 differentiation. Analysis of global gene expression of Tregs generated using low TGFb + harmine reveals significant similarity to Tregs generated using high TGFb only and suggests relevance of harmine-engaged mechanisms to IBD.
2015-04-29 | GSE64247 | GEO
Project description:Using an unbiased chemical biology approach, we discover harmine as a novel regulator of Treg/Th17 differentiation. Harmine enhances Treg differentiation (working in conjunction with low levels of exogenous TGFb) and inhibits Th17 differentiation. Analysis of global gene expression of Tregs generated using low TGFb + harmine reveals significant similarity to Tregs generated using high TGFb only and suggests relevance of harmine-engaged mechanisms to IBD.
2015-04-29 | GSE67960 | GEO
Project description:Transcriptional profiling of mouse Th17 cells comparing WT Th17 cells with Pten-deficient Th17 cells. Naïve CD4 T cells from each mice were cultured Th17 polarizing condition for 3 days. Goal was to determine the effects of Pten on global gene expression.
2017-08-10 | GSE102414 | GEO
Project description:To determine specific miRNAs for Th17 cells, we performed comparative miRNA screening of activated CD4+ T, polyclonal Th17 (Th17 poly) and OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures or Th17 Ag-sp sorted cells. The expression of miRNAs analyzed by microarray revealed 27 miRNAs exclusively expressed in culture or sorted Th17 Ag-sp cell subset.
2021-01-01 | GSE109992 | GEO
Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.
2020-05-26 | PXD010612 | Pride