The aim of this study was to identify differential gene expression in lung T cell subsets upon germline Serpinb1a ablation.
SerpinB1 regulates homeostatic expansion of IL-17+ γδ and CD4+ Th17 cells.
Specimen part
View SamplesThis study was designed to evaluate similarities and differences between transcriptional responses of developing Th17 cells to the prolyl-tRNA synthetase inhibitor, halofuginone, and the mTOR inhibitor, rapamycin. Further comparisons between wild-type and Gcn2-/- Th17 cells allow for investigation into which gene modules regulated by halofuginone or rapamycin treatment require Gcn2.
Halofuginone-induced amino acid starvation regulates Stat3-dependent Th17 effector function and reduces established autoimmune inflammation.
Specimen part
View SamplesThe aim of this study was to identify differentially-expressed genes in CCR4hi/CXCR3- and CCR4lo CXCR3+ CCR6+ human Th17 cell subsets
Pro-inflammatory human Th17 cells selectively express P-glycoprotein and are refractory to glucocorticoids.
No sample metadata fields
View SamplesThe aim of this study was to characterize the transcriptional signature of MDR1+ human memory T cells isolated from clinically inflamed gut tissue, and compare it to local MDR1- memory T cells
Pro-inflammatory human Th17 cells selectively express P-glycoprotein and are refractory to glucocorticoids.
Specimen part
View SamplesProtein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency.
Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents.
Specimen part, Treatment
View SamplesThe aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells.
Pharmacologic inhibition of RORγt regulates Th17 signature gene expression and suppresses cutaneous inflammation in vivo.
Specimen part, Treatment
View SamplesGenome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations
Toxic-selenium and low-selenium transcriptomes in Caenorhabditis elegans: toxic selenium up-regulates oxidoreductase and down-regulates cuticle-associated genes.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View SamplesNotch1 is a key regulator of endothelial cell behaviour. This experiment was designed to identify genes regulated by Notch1 signaling in inflammatory activated mouse endothelial cells.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View SamplesProinflammatory activation of endothelial cells leads to recruitment of leukocytes by upregulation of adhesion molecules and presentation of chemoattractants. In response to such activation there is also a strong shift in the endothelial expression of Notch ligands, with downregulation of Dll4 and a upregulation of JAG1. To assess whether Jagged1 would affect the endothelial activation profile, we suppressed JAG1 expression during IL-1-induced activation by means of siRNA and performed a genome-wide transcriptome analysis. Our results show for the first time that Jagged1 modulates the transcription profile of activated endothelial cells and describe data that imply a role for Jagged1 in sharpening the inflammatory profile of the vasculature, giving it an edge towards leukocyte recruitment. These findings imply that Jagged1 might be a potential therapeutic target to attenuate inflammation and reduce tissue damage in inflammatory diseases.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View Samples