Single-cell RNA-seq from Th17 cells differentiated in vitro under pathogenic (Th17p) and non-pathogenic (Th17n) conditions with high (25mM) or low (1mM) glucose media concentration
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE289733 | GEO | 2025/05/14
REPOSITORIES: GEO
Similar Datasets
Project description:Single-cell RNA-seq from Th17 cells differentiated in vitro under pathogenic (Th17p) and non-pathogenic (Th17n) conditions with high (25mM) or low (1mM) glucose media concentration
| PRJNA1224264 | ENA
Project description:We investigated the effect of glycolytic inhibitors on Th17 differentiation
2025-05-14 | GSE290297 | GEO
Project description:TGF-beta3 produced by developing Th17 cells induces highly pathogenic T cells that are functionally and molecularly distinct from TGF-beta1-induced Th17 cells. The microarray data represent a distinct molecular signature for pathogenic versus non-pathogenic Th17 cells. Total of seven groups with two to four samples per group from two independent experiments. The no cytokines group (Th0) was used as a control to normalize the data. 7 groups: B6: (IL-1beta, IL-6) B623: (IL-1beta, IL-6, IL-23) T16: (TGF-beta1, IL-6) T1623: (TGF-beta1, IL-6, IL-23) T36: (TGF-beta3, IL-6) T3623: (TGF-beta3, IL-6, IL-23) NOCYTO: no cytokines
2012-09-01 | E-GEOD-39820 | biostudies-arrayexpress
Project description:Chemokine receptor CCR6 is a G-protein-coupled receptor that binds its high-affinity ligand, CCL20. Among the CD4+ T cells, Th17 and regulatory T cells express CCR6, which facilitates their migration in CCL20-enriched, inflamed tissue. Migration of CCR6+ T cells from secondary lymphoid tissues into inflamed tissues exposes them to a distinct metabolic microenvironment. What drives the metabolic adaptation of cells in these tissues and what contributes to their effector or regulatory function is not clearly understood. During colitis, increased gut production of CCL20 promotes the recruitment of these cells. We demonstrated that the intrinsic signaling of CCL20-CCR6 in CD4+ T cells promotes the differentiation of inflamatory Th1-like Th17 cells (T-bet+RORγt+) during colitis in both mouse models and humans. This signaling induces rapamycin-sensitive phosphorylation of PI3K, Akt, mTORC1, and STAT3 in a CCR6-dependent manner. RNA-seq and proteomics analysis revealed alterations in CCL20 during Th17 differentiation, affecting several metabolic pathways, including energy metabolism. CCL20 significantly increased glycolysis and inhibited oxidative phosphorylation, thereby driving the differentiation of pathogenic Th17 cells. Our findings suggest that alterations in CCR6-induced changes in Th17 metabolism offer an interesting therapeutic target for gut inflammation and autoimmunity.
2025-12-10 | PXD071790 | Pride
Project description:TGF-beta3 produced by developing Th17 cells induces highly pathogenic T cells that are functionally and molecularly distinct from TGF-beta1-induced Th17 cells. The microarray data represent a distinct molecular signature for pathogenic versus non-pathogenic Th17 cells.
2012-09-01 | GSE39820 | GEO
Project description:Immunity to fungal infections is mediated by cells of the innate and adaptive immune system. Activation of immune cells requires Ca2+ influx through the Ca2+ channel ORAI1, which is activated by stromal interaction molecule 1 (STIM1). Th17 cells are essential for immunity to C. albicans infection and require Ca2+ influx for expression of IL-17A and other Th17 cytokines. In mice, deletion of STIM1 and thus Ca2+ influx in all immune cells enhanced susceptibility to mucosal C. albicans infection, whereas T cell-specific deletion of STIM1 impaired immunity to systemic C. albicans infection. STIM1 deletion in CD4 T cells had different effects on gene expression programs in pathogenic (proinflammatory) and non-pathogenic Th17 cells. STIM1 deletion in non-pathogenic Th17 cells, which are required for antifungal immunity, compromised the expression of genes in several metabolic pathways including Foxo and HIF-1a signaling as well as the TCA cycle and oxidative phosphorylation (OXPHOS). Consequently, STIM1 deficient non-pathogenic Th17 cells had impaired glycolysis and mitochondrial respiration. By contrast, STIM1 deletion in pathogenic Th17 cells showed only attenuated mitochondrial function but normal glycolysis.
2020-06-01 | GSE149162 | GEO
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. Effects of NaCl on Th17 differentiation
2013-03-07 | E-GEOD-43957 | biostudies-arrayexpress
Project description:In vitro differentiated Th17 have a distinct expression profile compared to in vivo differentiated Th17 Several conditions of Th17 cells were tested, with 2-3 replicates per condition.
2015-04-18 | E-GEOD-68017 | biostudies-arrayexpress
Project description:Th17 cells are key players in autoimmune diseases. However, the roles of non-coding RNAs in Th17 cells are largely unknown. Here, we show that deletion of the Dicer gene specifically in Th17 cells protects from experimental autoimmune encephalomyelitis (EAE). Th17 cells highly express the miR-183/96/182 cluster (miR-183C), in response to IL-6/STAT3 signaling. Moreover, miR-183C regulates pathogenic cytokine expression during Th17 development. Furthermore, transcription factor Foxo1 is one of functional targets of miR-183C in Th17 cells: Foxo1 negatively regulates the pathogenicity of Th17 cells and miR-183C represses Foxo1 expression. Collectively, our results demonstrate one of crucial roles for miR-183C cluster in regulation of Th17 cell function in autoimmune diseases.
2016-06-21 | GSE78505 | GEO
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