Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA291926 | ENA |
REPOSITORIES: ENA
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Project description:The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we compared the signature found between unrelated healthy controls and non-diabetic cystic fibrosis patients possessing Pseudomonas aeruginosa pulmonary tract infection. UPN727 cells were stimulated with autologous plasma (n=5), unrelated healthy control plasma (n=24), or plasma from patients with cystic fibrosis possessing Psuedomonas aeruginosa pulmonary tract infection (n=20). Gene expression analysis was perfromed in order to evaluate the transcriptional signature associated with cystic fibrosis.
2012-09-01 | E-GEOD-35711 | biostudies-arrayexpress
Project description:The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we apply this approach to inflammatory bowel disease by examining groups of Crohn's disease (CD) and ulcerative colitus (UC) patients. The induced plasma induced signatures are compared to those of Type 1 diabetes patients (RO T1D) as well as unrelated healthy controls (uHC).
2015-10-01 | GSE71730 | GEO
Project description:Small, soluble metabolites are not only essential intermediates in intracellular biochemical processes, but can also influence neighboring cells when released into the extracellular milieu. Here, we identify the metabolite and neurotransmitter GABA as a candidate signaling molecule synthesized and secreted by activated B cells and plasma cells. We show that B cell-derived GABA promotes monocyte differentiation into anti-inflammatory macrophages which secrete IL-10 and inhibit CD8+ T cell killer function. In mice, B cell deficiency or B cell-specific inactivation of the GABA generating enzyme GAD67 enhances anti-tumor responses. Our study reveals that in addition to cytokines and membrane proteins, small metabolites derived from B lineage cells have immunoregulatory functions, which may be pharmaceutical targets allowing fine-tuning of immune responses.
2021-11-15 | PXD028403 | Pride
Project description:The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we compared the signature found between unrelated healthy controls and non-diabetic cystic fibrosis patients possessing Pseudomonas aeruginosa pulmonary tract infection.
2019-01-01 | GSE71799 | GEO
Project description:The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we compared the signature found between unrelated healthy controls and non-diabetic cystic fibrosis patients possessing Pseudomonas aeruginosa pulmonary tract infection.
2012-09-01 | GSE35711 | GEO
Project description:The plasma levels of tissue-specific microRNAs can be used as prognostic and diagnostic biomarkers for chronic and acute diseases. Thereby, the combination of diverse miRNAs into biomarker signatures using multivariate statistics seems especially powerful in view to tissue and condition specific miRNA shedding into the plasma. Although Next-Generation Sequencing (NGS) technology enables to analyse circulating microRNAs on a genome-scale level, it suffers from potential biases (e.g. adapter ligation bias) and lacks absolute transcript quantitation. In order to develop a robust NGS discovery assay for genome-scale quantitation of circulating microRNAs we first evaluated the sensitivity, repeatability and ligation bias of four commercially available small RNA library preparation protocols. The protocol from RealSeq Biosciences was selected based on its performance and usability, and coupled with a novel panel of exogenous small RNA spike-in controls to enable absolute quantitation and ensure comparability of data across independent NGS experiments. The established MicroRNA Next-Generation-Sequencing Discovery Assay (miND) was validated for its relative accuracy, precision, analytical measurement range and sequencing bias and was considered fit-for-purpose for microRNA biomarker discovery. Summarized, all these criteria were met and thus our analytical platform is considered fit-for-purpose for microRNA biomarker discovery from plasma, serum, cerebrospinal fluid (CSF), synovial fluid (SF), or extracellular vesicles (EV) extracted from cell culture medium in the setting of any diagnostic, prognostic or patient stratification need.
2022-01-20 | GSE189930 | GEO
Project description:Total RNA from 59 human plasma samples was used to generate signatures of extracellular vesicles used as basis for evaluation of potential disease states
2024-01-17 | GSE217159 | GEO
Project description:IL-27 is an immunoregulatory cytokine whose essential function is to limit immune responses. We found that the gene encoding cholesterol 25-hydroxylase (Ch25h) was induced in CD4+ T cells by IL-27, enhanced by TGF-β, and antagonized by T-bet. Ch25h catalyzes cholesterol to generate 25-hydroxycholesterol (25OHC), which was subsequently released to the cellular milieu, functioning as a modulator of T cell response. Extracellular 25OHC suppressed cholesterol biosynthesis in T cells, inhibited cell growth, and induced nutrient-deprivation cell death without releasing high-mobility group box-1. This growth inhibitory effect was specific to actively proliferating cells with high cholesterol demand and was reversed when extracellular cholesterol was replenished. Interestingly, Ch25h expressing CD4+ T cells that received IL-27 and TGF-β signals became refractory to 25OHC-mediated growth inhibition in vitro. Nonetheless, IL-27 treated T cells negatively affected viability of bystander cells in a paracrine manner, but only if the bystander cells were in the early phases of activation. In mouse models of skin inflammation due to autoreactive T cells or chemically induced hypersensitivity, genetic deletion of Ch25h or Il27ra led to worsened outcomes. Thus, Ch25h is an immunoregulatory metabolic switch induced by IL-27 and dampens excess bystander T effector expansion in tissues through its metabolite derivative, 25OHC. This study reveals regulation of cholesterol metabolism as a modality for controlling tissue inflammation and thus represents a mechanism underlying T cell immunoregulatory functions.
2021-10-08 | GSE176039 | GEO
Project description:IL-27 is an immunoregulatory cytokine whose essential function is to limit immune responses. We found that the gene encoding cholesterol 25-hydroxylase (Ch25h) was induced in CD4+ T cells by IL-27, enhanced by TGF-β, and antagonized by T-bet. Ch25h catalyzes cholesterol to generate 25-hydroxycholesterol (25OHC), which was subsequently released to the cellular milieu, functioning as a modulator of T cell response. Extracellular 25OHC suppressed cholesterol biosynthesis in T cells, inhibited cell growth, and induced nutrient-deprivation cell death without releasing high-mobility group box-1. This growth inhibitory effect was specific to actively proliferating cells with high cholesterol demand and was reversed when extracellular cholesterol was replenished. Interestingly, Ch25h expressing CD4+ T cells that received IL-27 and TGF-β signals became refractory to 25OHC-mediated growth inhibition in vitro. Nonetheless, IL-27 treated T cells negatively affected viability of bystander cells in a paracrine manner, but only if the bystander cells were in the early phases of activation. In mouse models of skin inflammation due to autoreactive T cells or chemically induced hypersensitivity, genetic deletion of Ch25h or Il27ra led to worsened outcomes. Thus, Ch25h is an immunoregulatory metabolic switch induced by IL-27 and dampens excess bystander T effector expansion in tissues through its metabolite derivative, 25OHC. This study reveals regulation of cholesterol metabolism as a modality for controlling tissue inflammation and thus represents a mechanism underlying T cell immunoregulatory functions.
2021-10-07 | GSE175494 | GEO
Project description:We utilized FAIRE-seq to identify accesible chromatin in mouse embryonic-, epiblast-, and neural- stem cells in addition to mouse embryonic fibroblasts. Analysis of these data sets reveal cell type specific chromatin signatures that differentiate naïve and primed pluripotency. Functional analysis of type-specific peaks revealed cell-type specific enhancers. FAIRE-seq of mESC, EpiSC, NSC and MEF
2015-01-01 | E-GEOD-58520 | biostudies-arrayexpress