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Transcriptome profile of peripheral blood mononuclear cells in patients with type I diabetes and their first grade relatives

ABSTRACT: Type 1 Diabetes (T1D) is considered to be a Th1 autoimmune disease characterised by an absolute lack of insulin caused by an autoimmune destruction of the insulin producing pancreatic beta cells. Th1 lymphocytes are responsible for the infiltration of the islets of Langerhans and for the cytokine release that supports cytotoxic (Tc) lymphocytes to mediate destruction of the beta cells. The preclinical disease stage is characterized by the generation of the self-reactive lymphocytes that infiltrate the pancreas and selectively destroy the insulin-producing beta cells present in the islets. Other cellular immune mechanisms regarding immunoregulation and antigen presentation and processing are involved in T1D pathogenesis as well. Our aim was to identify genes involved in the corresponding signalling cascades, especially those which may serve as promising diagnostic tools for the identification of persons in the prediabetic phase of the disease. We addressed the question by analysing gene expression profiles of freshly isolated peripheral blood mononuclear cells in type 1 diabetes patients, their first degree relatives divided according to their autoantibody status, and healthy controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29142 | GEO | 2011/05/09

SECONDARY ACCESSION(S): PRJNA140345

REPOSITORIES: GEO

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Transcriptome profile of peripheral blood mononuclear cells in patients with type I diabetes and their first grade relatives

Project description:Type 1 Diabetes (T1D) is considered to be a Th1 autoimmune disease characterised by an absolute lack of insulin caused by an autoimmune destruction of the insulin producing pancreatic beta cells. Th1 lymphocytes are responsible for the infiltration of the islets of Langerhans and for the cytokine release that supports cytotoxic (Tc) lymphocytes to mediate destruction of the beta cells. The preclinical disease stage is characterized by the generation of the self-reactive lymphocytes that infiltrate the pancreas and selectively destroy the insulin-producing beta cells present in the islets. Other cellular immune mechanisms regarding immunoregulation and antigen presentation and processing are involved in T1D pathogenesis as well. Our aim was to identify genes involved in the corresponding signalling cascades, especially those which may serve as promising diagnostic tools for the identification of persons in the prediabetic phase of the disease. We addressed the question by analysing gene expression profiles of freshly isolated peripheral blood mononuclear cells in type 1 diabetes patients, their first degree relatives divided according to their autoantibody status, and healthy controls. 9 T1D-patients versus 10 first degree relatives versus 10 healthy controls

2011-05-09 | E-GEOD-29142 | biostudies-arrayexpress

microRNAs of thymocytes and of peripheral and pancreas-infiltrating T lymphocytes

Project description:As early as one month of age, nonobese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes, which destruct insulin-producing beta cells, producing autoimmune diabetes mellitus (T1D) within eightmonths. Thus, we hypothesized that during the development of T1D, the transcriptional modulation of immune reactivity genes may occur as thymocytes mature into peripheral T lymphocytes. The transcriptome of thymocytes and peripheral CD3+ T lymphocytes from prediabetic or diabetic mice analyzed through microarray hybridizations identified the differentially expressed genes.

2012-07-31 | E-MEXP-3572 | biostudies-arrayexpress

CITEseq of lymphocytes from pancreatic lymph nodes, mesenteric lymph nodes, and spleen from 20 Human Pancreas Analysis Program (HPAP) donors

Project description:Type 1 diabetes (T1D) is caused by the autoimmune destruction of insulin-producing pancreatic beta cells, leading to life-long dependence on exogenous insulin. Profiling immune cells that infiltrate islets would be invaluable to understanding how beta cell destruction occurs. However, human pancreatic samples demonstrating active infiltration and beta cell destruction are rare. Alternatively, peri-pancreatic lymph nodes (pLNs) or other secondary lymphoid organs may harbor immune cells which participate in memory responses that drive T1D autoimmunity. To study the immune response throughout T1D onset and disease, lymphocytes from pLNs, mesenteric lymph nodes (mesLNs), and the spleen were collected from human T1D, auto-antibody positive (AAb+), and normal donors (NDs) enrolled in the Human Pancreas Analysis Program (HPAP). Tissue immune cell identity, phenotype, and transcriptional status was analyzed using Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITEseq). Lymphocytes from 20 pLN, 12 mesLN, and 18 spleen samples spanning 6 ND, 7 AAb+, and 7 T1D donors were thawed and processed through the CITEseq pipeline. At least 5 donors per disease group had a paired pLN and spleen sample, with at least 3 of the 5 donors per disease group having a paired mesLN sample, allowing for cross-tissue immune status comparison spanning multiple stages of disease onset. The dataset provides one of the first and largest CITEseq datasets on human AAb+ and T1D samples publicly available.

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Effects of exosomes from T lymphocytes of NOD mice on pancreatic islet-cell gene expression

Project description:During Type 1 diabetes development, T lymphocytes infiltrate pancreatic islets and induce the destruction of the insulin-producing cells within the islets, the beta-cells. T lymphocytes are known to secrete pro-inflammatory cytokines but also exosomes that could contribute to the mechanisms leading to beta-cell death. In this project, we wanted to investigate the effect of exosomes released from T lymphocytes on beta-cell gene expression.

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Assessing the role of microRNAs in post-transcriptional control of thymocytes and peripheral lymphocytes in NOD mice

Project description:As early as one month of age, non-obese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes, which destruct insulin-producing beta cells, leading to autoimmune diabetes mellitus (T1D) within eight months. Thus, we hypothesized that during the development of T1D, the transcriptional modulation of immune reactivity genes, as well as, modulation of microRNAs (miRNAs) may occur during thymocytes mature into peripheral CD3+ T lymphocytes. Our aim is to analyze the transcriptional modulation of mRNA and microRNAs during development of thymocytes into peripheral CD3+ T lymphocytes in the context of the emergence of T1D.

2011-07-01 | E-MEXP-3235 | biostudies-arrayexpress

Transcription profiling human whole blood from children with pre-type1diabetes

Project description:Type 1 diabetes (T1D) is an autoimmune disease caused by selective destruction of insulin producing pancreatic beta-cells in the islets of the Langerhans. The progression to clinical diabetes is characterized by the appearance of autoantibodies against islet cells (ICA) and beta-cell-specific antigens (IAA, IA-2 and GADA), which are considered the first markers signifying onset of autoimmunity. The mechanisms initiating or enhancing the autoimmune process remain poorly understood. Transcriptomic profiling on whole blood samples provides an approach for monitoring T1D disease process. In these investigations of pathways that are changed during the disease process, we have analyzed RNA from longitudinal peripheral blood samples of children who have developed T1D associated autoantibodies and eventually clinical type 1 diabetes . All study subjects were participants of the Type 1 Diabetes Prediction and Prevention (DIPP) study in Finland (38). Whole-blood RNA samples were collected during periodic clinic visits, typically at 3 to 12 month intervals. 2.5 ml venous blood was drawn into PAXgene Blood RNA tubes (Becton-Dickinson) and stored at -70°C. T1D-associated autoantibodies were measured from blood samples taken at each visit. Prospective samples from 3 children who developed T1D (subjects T1D_1 - T1D_3) and 2 children who developed ICA (subjects ICA_1 and ICA_2) during the DIPP follow-up were selected to the present study. Control children for the T1D cases (subjects T1D_C1 - T1D_C2) were matched for age, gender, birth place and HLA-genotype, from families who have no first-degree relatives with T1D. All samples (n=60) were processed and hybridized on Affymetrix Human Genome U133 Plus 2.0 arrays.

2010-03-31 | E-TABM-666 | biostudies-arrayexpress

m6A RIP-seq for Cytokine-treated Islets and Beta-cells or T1D Islets

Project description:Type 1 Diabetes (T1D) is characterized by autoimmune-mediated destruction of insulin-producing beta-cells. Recent research has focused on the role of the innate immune system in initiating this process. To investigate this further, we used m6A-profiling of human islets from non-diabetic individuals and the human beta-cell line EndoC-bH1 treated with PBS or interleukin 1 beta and interferon alpha, as well as established T1D patients. Our findings reveal that N6-Methyladenosine (m6A) is a mechanism that helps protect beta-cells by accelerating the decay of mRNA from the 2'-5'-oligoadenylate synthetase (OAS) genes, which controls the antiviral innate immune response at the onset of T1D. These results provide insight into the adaptive safeguarding mechanisms of beta-cells and the role of m6A in T1D development, highlighting potential targets for therapeutic interventions.

2024-01-01 | GSE228267 | GEO

Genetic predisposition for beta cell fragility underlies type 1 and type 2 diabetes

Project description:Type 1 and type 2 diabetes (T1D and T2D) share pathophysiological characteristics, yet mechanistic links have remained elusive. T1D results from autoimmune destruction of pancreatic beta cells, while beta cell failure in T2D is delayed and progressive. Here we find a new genetic component of diabetes susceptibility in T1D non-obese diabetic (NOD) mice, identifying immune-independent beta cell fragility. Genetic variation in Xrcc4 and Glis3 alter the response of NOD beta cells to unfolded protein stress, enhancing the apoptotic and senescent fates. The same transcriptional relationships were observed in human islets, demonstrating the role for beta cell fragility in genetic predisposition to diabetes.

2016-02-24 | PXD000859 | Pride

NET proteome of neutrophils from people with long-standing type 1 diabetes and healthy control

Project description:Type 1 diabetes (T1D) is a chronic T-cell-mediated autoimmune disease, leading to the destruction of the pancreatic insulin-producing beta cells. Little is known about the involvement of neutrophils that exert multifaceted functions like phagocytosis, degranulation, production of cytokines and the formation of neutrophil extracellular traps (NETosis), in the pathogenesis of T1D. Our aim was to gain insight into the proteome of neutrophils undergoing NETosis from patients with long-standing T1D compared to age- and sex-matched healthy controls under both resting and stimulated conditions (phorbol-myristate acetate, PMA, 100nM; ionomycin, 20µM; 3hours) by LC/MS-MS.

2023-05-15 | PXD033599 | Pride

Proteome and (ox)PTP profile analysis of diabetic NOD mouse under single (anti-CD3) or combined (anti-CD3 + IL1RA) treatment

Project description:Type 1 diabetes (T1D) results from autoimmune destruction of β cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas of diabetic NOD mice treated with anti-CD3 mAb and IL-1RA combination therapy. The treatment reversed hyperglycemia compared to the anti-CD3 alone control group. We observed enhanced expression of PTPN2, a T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the islets from cured mice.

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