Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

11 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of in vitro-generated murine T helper 17 cells

ABSTRACT: T helper (Th) 17 cells form a T cell subset which is crucial to maintain immunity against extracellular bacteria and fungi at epithelial barriers, but Th17 cells are also enriched at sites of inflammation in autoimmune disease. These sites are commonly characterised by adverse environmental conditions which are prone to trigger an ER (endoplasmic reticulum)-stress response. Our lab recently observed that the ER-stress response can be a strong driving force for Th17 cell differentiation. The aim of this RNA-seq project was to characterise the novel Th17 cell population generated by IL-6 and cyclopiazonic acid (CPA)-induced ER stress by transcriptional profiling of ER-stress generated and conventional Th17 cells. For this purpose nave IL17A-Cre Rosa-RFP CD4 T cells were cultured with a combination of Interleukin 6 with Transforming growth factor (TGF) or CPA for three days. Then, RFP-positive Th17 cells from four different experiments were enriched for by FACS sorting. Following RNA isolation using QIAGEN's RNA Mini Plus Kit and rRNA depletion accomplished with the NEBNext rRNA Depletion Kit, RNA-seq libraries were generated using the undirectional NEBNext Ultra RNA Library Prep Kit for Illumina. The libraries were sequenced as 75bp paired-end reads on a NextSeq 500 sequencer and analysed using QIAGEN's Biomedical Workbench.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Marc Veldhoen

PROVIDER: E-MTAB-5692 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Human chorionic gonadotropin promotes murine Treg cells and restricts pregnancy-harmful proinflammatory Th17 responses – proteomics data

Project description:In this study, the participation of fetal factors in maintaining the immune balance during gestation was investigated by assessing the effects of human chorionic gonadotropin (hCG) on murine Treg cells and Th17 cells.

2022-10-14 | PXD035883 | Pride

Chemical Inhibition of the ROR?t-dependent Transcriptional Network in Th17 cells [RNA-Seq]

Project description:ROR?t is a transcription factor required for T helper 17 (Th17) cell development. We identified three ROR?t-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized ROR?t binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and ROR?t-deficient cells. ROR?t is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced ROR?t from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. Transcriptional profiling of Th17 cells under chemical perturbations of ROR?t, DMSO, and knockout of ROR?t

2014-04-17 | E-GEOD-56018 | biostudies-arrayexpress

Comparative transcriptome analysis of Th22 and Th17 cells

Project description:Microarray was used to delineate the global gene expression profile underlying the specific developmental program of two divergent antigen-specific T helper subsets (Th22 versus Th17) by identifying upregulation or downregulation of key lineage-determining transcription factors, cytokines, chemokines and other genes that govern their functional attributes. To identify factors that might distinguish the Th22 and Th17 developmental programs, comparative global transcriptome analysis between these 2 subsets was performed. Naïve splenic CD4+ T cells from OT-II-transgenic mice were isolated and grown in vitro under T-helper lineage-specific conditions in the presence of cognate antigen (ovalbumin) to identify their distinctive global gene-regulation profiles.

2013-01-29 | E-GEOD-42332 | biostudies-arrayexpress

Transcriptional profiling of Th17gene expression in Map3k1 control and mutant mice

Project description:Mapks are regulators of T cell proliferative expansion and cell cycle progression. Genetic analysis of Th17 cells in Map3k1ÎKD and control mice will demonstrate whether Mekk1 (encoded by Map3k1) signaling activates Jnks to regulate cell cycle molecules and proliferative expansion. Comparative transcriptional profiling of Th17 molecular expression between experimental and control genotypes will reveal molecular targets that could play a role in the Map3k1-dependent mechanisms underlying proliferation.

2016-08-31 | E-MTAB-4499 | biostudies-arrayexpress

Chemical Inhibition of the RORγt-dependent Transcriptional Network in Th17 cells [RNA-Seq 2]

Project description:RORγt is a transcription factor required for T helper 17 (Th17) cell development. We identified three RORγt-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized RORγt binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and RORγt-deficient cells. RORγt is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced RORγt from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. Transcriptional profiling of Th17 cells under chemical perturbations of RORγt, DMSO, and knockout of RORγt. It includes repeats for all the data in GSE56018, plus one additional condition.

2014-04-17 | E-GEOD-56240 | biostudies-arrayexpress

Chemical Inhibition of the RORγt-dependent Transcriptional Network in Th17 cells [ChIP-Seq]

Project description:RORγt is a transcription factor required for T helper 17 (Th17) cell development. We identified three RORγt-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized RORγt binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and RORγt-deficient cells. RORγt is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced RORγt from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. DNA binding of RORγt in WT Th17 cells and under chemical perturbations of RORγt; Additional data is included for epitope-tagged exogenous RORγt in EL4 cells (a murine lymphoma cell line)

2014-04-17 | E-GEOD-56019 | biostudies-arrayexpress

Induction of pathogenic Th17 cells by salt inducible kinase SGK-1 (SGK-1 KO)

Project description:Th17 cells are highly proinflammatory cells that are critical for clearing extracellular pathogens like fungal infections and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and endowing Th17 cells with pathogenic effector functions2. Previous studies have shown that IL-23 signaling reinforces the Th17 phenotype by increasing expression of IL-23 receptor (IL-23R)3. However, the precise molecular mechanism by which IL-23 sustains the Th17 response and induces pathogenic effector functions has not been elucidated. Here, we used unbiased transcriptional profiling of developing Th17 cells to construct a model of their signaling network and identify major nodes that regulate Th17 development. We identified serum glucocorticoid kinase-1 (SGK1), as an essential node downstream of IL-23 signaling, critical for regulating IL-23R expression and for stabilizing the Th17 cell phenotype by deactivation of Foxo1, a direct repressor of IL-23R expression. A serine-threonine kinase homologous to AKT4, SGK1 has been associated with cell cycle and apoptosis, and has been shown to govern Na+ transport and homeostasis5, 6 7, 8. We here show that a modest increase in salt (NaCl) concentration induces SGK1 expression, promotes IL-23R expression and enhances Th17 cell differentiation in vitro and in vivo, ultimately accelerating the development of autoimmunity. The loss of SGK1 resulted in abrogation of Na+-mediated Th17 differentiation in an IL-23-dependent manner. These data indicate that SGK1 is a critical regulator for the induction of pathogenic Th17 cells and provides a molecular insight by which an environmental factor such as a high salt diet could trigger Th17 development and promote tissue inflammation. Th17 cells; comparing Sgk1-/- to WT

2013-03-07 | E-GEOD-43956 | biostudies-arrayexpress

Transcription profiling of mouse spleen CD4+ CD44Low CD62LHigh cells stimulated with anti-CD3 or anti-CD28 in the presence or absence of hTGFb-1 and mouse IL-6

Project description:Mouse spleen CD4+CD44LowCD62LHigh cells were stimulated with 2ug/ml anti-CD3(eBioscience), 2ug/ml anti-CD28 (eBioscience) in the presence (Th17 condition) or absence (Th0 condition) of hTGFb-1 (1ng/ml eBioscience), mouse IL-6(10ng/ml eBioscience). Cells were collected after 24 hourÕs culture using RNAeasy columns (Qiagen) for total RNA isolation. Isolated total RNA from Th0 and Th17 conditioned cells were submitted for the microarray gene transcription comparison analysis using Affymetrix Mouse 430A 2.0 array chips.

2008-12-21 | E-TABM-583 | biostudies-arrayexpress

Reconstruction of the dynamic regulatory network that controls Th17 cell differentiation by systematic perturbation in primary cells (Th17 differentiation timecourse)

Project description:Despite their enormous importance, the molecular circuits that control the differentiation of Th17 cells remain largely unknown. Recent studies have reconstructed regulatory networks in mammalian cells, but have focused on short-term responses and relied on perturbation approaches that cannot be applied to primary T cells. Here, we develop a systematic strategy – combining transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based tools for performing gene perturbations in primary T cells – to derive and experimentally validate a temporal model of the dynamic regulatory network that controls Th17 differentiation. The network is arranged into two self-reinforcing and mutually antagonistic modules that either suppress or promote Th17 differentiation. The two modules contain 12 novel regulators with no previous implication in Th17 differentiation, which may be essential to maintain the appropriate balance of Th17 and other CD4+ T cell subsets. Overall, our study identifies and validates 39 regulatory factors that are embedded within a comprehensive temporal network and identifies novel drug targets and organizational principles for the differentiation of Th17 cells. Time course microarray data for Th17 differentiation, including Th0 control

2013-03-07 | E-GEOD-43955 | biostudies-arrayexpress

Differential Regulation of Th17 and Th1 Cells in mouse by Glutaminase-Dependent Metabolism and Chromatin Remodeling

Project description:Activated T cells differentiate into functional subsets which require distinct metabolic programs. Glutaminase (GLS) converts glutamine to glutamate to provide substrate for the tricarboxylic acid cycle and epigenetic reactions and here we identify a key role for GLS in T cell activation and specification. Though GLS-deficiency diminished T cell activation, proliferation and impaired differentiation of Th17 cells, loss of GLS also increased Tbet and Interferon-γ expression and CD4 Th1 and CD8 CTL effector cell differentiation. These changes were mediated by differentially altered gene expression and chromatin accessibility, leading to increased sensitivity of Th1 cells to IL-2 mediated mTORC1 signaling. In vivo, GLS-null T cells failed to drive a Th17 mediated Graft-vs-Host Disease model. Transient inhibition of GLS, however, increased Th1 and CTL T cell numbers in viral and chimeric antigen receptor models. Glutamine metabolism thus has distinct roles to promote Th17 but constrain Th1 and CTL effector cell differentiation.

2018-09-01 | E-MTAB-6648 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data