Expression data from peripheral blood mononuclear cells（PBMCs) in newly diagnosed type 2 diabetes
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PROVIDER: PRJNA707418 | ENA |
REPOSITORIES: ENA
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Project description:Type 1 diabetes mellitus (T1D) is a common autoimmune disease mediated by autoimmune attack against pancreatic b cells.Dys-regualtion of the component of peripheral blood mononuclear cells (PBMCs), including T-cells and B-cells, and smaller amounts of NK cells and dendritic cells, have all been implicated in this process This study sought to identify T1D associated differently expressed genes in the peripheral blood mononuclear cell (PBMC). Peripheral blood mononuclear of newly diagnosed type1 diabetes patients and normal controls were purified by LymphoprepTm gradient purification according to the manufacturer’s instructions (Axis-Shield PoC AS, Oslo, Norway) for futher microarray analysis.
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Project description:Objective: We hypothesized that type 1 diabetes (T1D) is accompanied by changes in gene expression in peripheral blood mononuclear cells (PBMCs) due to dysregulation of adaptive and innate immunity, counterregulatory responses to immune dysregulation, insulin deficiency and hyperglycemia. Research Design and Methods: Microarray analysis was performed on PBMCs from 43 patients with newly diagnosed T1D, 12 patients with newly diagnosed type 2 diabetes (T2D) and 24 healthy controls. One and four month follow-up samples were obtained from 20 of the T1D patients. Results: Microarray analysis identified 282 genes differing in expression between newlydiagnosed T1D patients and controls at a false discovery rate of 0.05. Changes in expression of interleukin-1β (IL1B), early growth response gene 3 (EGR3), and prostaglandin-endoperoxide synthase 2 (PTGS2) resolved within four months of insulin therapy and were also observed in T2D suggesting that they resulted from hyperglycemia. With use of a knowledge base, 81/282 genes could be placed within a network of interrelated genes with predicted functions including apoptosis and cell proliferation. IL1B and the MYC oncogene were the most highly-connected genes in the network. IL1B was highly overexpressed in both T1D and T2D, whereas MYC was dysregulated only in T1D. Conclusion: T1D and T2D likely share a final common pathway for beta cell dysfunction that includes secretion of interleukin-1β and prostaglandins by immune effector cells, exacerbating existing beta cell dysfunction, and causing further hyperglycemia. The results identify several targets for disease-modifying therapy of diabetes and potential biomarkers for monitoring treatment efficacy. Keywords: Diabetes, microarray analysis, peripheral blood mononuclear cells
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Project description:Autologous nonmyeloablative hematopoietic stem cell transplantation (AHST) was the first therapeutic approaches that can improve beta cell function in type 1 diabetic (T1D) patients. This study was designed to investigate the potential mechanisms involved.We applied AHST to nine T1D patients diagnosed within six months and analyzed the acute response in peripheral blood genomic expression profiling at the six-month follow-up. Peripheral blood mononuclear of newly diagnosed type1 diabetes patients at diagnosis and at six months post-transplantation by autologous peripheral stem cell were purified by LymphoprepTm gradient purification according to the manufacturer's instructions (Axis-Shield PoC AS, Oslo, Norway) for futher microarray analysis.
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Project description:Peste des Petits Ruminants (PPR) is a highly infectious disease caused by a virus of the genus Morbillivirus (PPRV), infecting mainly sheep and goat. Susceptibility of host can vary widely with host breed and virus strain. The mechanisms underlying this variability are not well understood. Here, we carried out the first comparative in vitro study on goat peripheral blood mononuclear cells (PBMCs) infected with PPRV strains of different virulence, vaccine strain (N75/1), low- (IC89), and high-virulent strain (MA08). Goat PBMCs were infected by the different strains and stimulated with Concanavalin A (Con A), and proteome changes of these cells were evaluated during the infection. The level of PPRV replication was assessed first by RT-qPCR quantification of viral N mRNA and by labelling the viral N protein inside the cells with specific antibodies and analysed by flow cytometry. The dynamics of PBMC sub-populations were also evaluated by flow cytometry. Our results showed that viral replication is critical for PPRV inhibitory effect on PBMCs proliferation. Highly virulent MA08 strain reached a higher level of replication in ConA-stimulated PBMCs and induced higher mortality compared to other strains. Low-virulent IC89 strain showed the lower replication level and cell proliferative inhibitory capacities. Differences in immune genes expression levels were assessed using RNAseq analysis and protein expression was compared using mass spectrometry. Analysis of these data provided the transcriptional and proteome landscape of PBMCs infected with these strains. The possible association between the transcriptional and proteome landscape and changes in immune cell subpopulations dynamics was explored.
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Project description:Genome-Scale draft model for Human Peripheral Blood Mononuclear Cells (PBMCs). A GEM for PBMCs was developed by applying the INIT
algorithm on Human Metabolic Reconstruction (HMR 2.0) as a template model. GEMs were contextualised/ constrained for different conditions using expression datasets. The gene/transcript expression data obtained from PBMCs of Type 1 Diabetes progressors, non-progressors, and healthy controls were employed to score each reaction of HMR 2.0. For further detail please refer to Electronic Supplementary Information of Sen et.al, Metabolic alterations in immune cells associate with progression to type 1 diabetes, Diabetologia, 15/01/2020, (https://doi.org/10.1007/s00125-020-05107-6).
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