Treg fitness signatures as a biomarker for disease activity in Juvenile Idiopathic Arthritis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE289068 | GEO | 2025/02/12
REPOSITORIES: GEO
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Project description:Children with oligoarticular JIA (arthritis in 4 or fewer joints) can either continue to have this mild form of arthritis (persistent oligoarticular JIA) or extend to a more sever form involving more than 4 joints (extended oligoarticular JIA) Synovial fluid mononuclear cell RNA was prepared from 21 recently diagnosed pre-treatment patients and grouped according to whether the patient had extended or persisted at one year after diagnosis
2009-03-04 | GSE15083 | GEO
Project description:The purpose of this study was to investigate the transcriptomic heterogeneity in synovial tissue of JIA patients
2024-05-25 | GSE253553 | GEO
Project description:Children with oligoarticular JIA (arthritis in 4 or fewer joints) can either continue to have this mild form of arthritis (persistent oligoarticular JIA) or extend to a more sever form involving more than 4 joints (extended oligoarticular JIA) Synovial fluid mononuclear cell RNA was prepared from 21 recently diagnosed pre-treatment patients and grouped according to whether the patient had extended or persisted at one year after diagnosis Each sample was hybridized to Affymetrix HGU133plus2 microarrays. The mean for each probeset was compared between groups in order to find differentially expressed genes whose expression might predict outcome in a prospective study
2009-03-04 | E-GEOD-15083 | biostudies-arrayexpress
Project description:Juvenile idiopathic arthritis (JIA) refers to any type of chronic arthritis that develops before the age of sixteen, lasts longer than six weeks, and has an unknown etiology. The existing diagnostic techniques for JIA are conventional and occasionally ineffective at distinguishing JIA from other pediatric illnesses because of their low specificity. This study was a comparative cross-sectional investigation finding prospective future biomarker candidates in JIA patients. A label-free mass spectrometry and bioinformatics tool were used in this study to examine the functional importance of proteins which were differentially expressed in JIA patients compared to their healthy counterparts. Receiver operating characteristic (ROC) curves were used to evaluate the predictive power of screened proteins, and they were validated in a different cohort using ELISA and Western blot analysis. It has been discovered that the JIA group has higher expression of two DEPs (Differentially Expressed Proteins), namely Myosin light chain 12b (Myl12b) and Mannose-binding lectin serine protease1 (MASP1) which showed good predictive abilities in ROC analysis. According to our research, these two proteins upregulated in JIA, Myl12b and MASP1, may serve as biomarkers for the diagnosis and treatment approaches of JIA.The study was a comparative cross-sectional study. The samples were obtained from a tertiary care hospital after obtaining approval from Institutional ethics committee.Samples were screened based on ILAR categorization criteria and the homogeneity of their preliminary biochemical evaluations. EDTA blood samples were collected from diagnosed active poly JIA patients. Plasma was separated, and highly abundant proteins were depleted using immunoaffinity techniques to enrich low-abundance proteins. After immune depletion, the proteins were concentrated, quantitated and normalised to 1mg/ml. The normalised samples underwent mass spectrometric analysis to identify low-abundance plasma proteins.The mass spectrometric analysis revealed several differentially expressed low-abundance plasma proteins in JIA patients. This research could pave the way for improved diagnostic and prognostic tools, as well as potential therapeutic targets for JIA, ultimately contributing to better patient outcomes.
2025-02-14 | PXD058863 | Pride
Project description:With H3K27ac chromatin immunoprecipitation we identified a disease-specific, inflammation-associated, (super-)enhancer signature in JIA patient synovial fluid-derived CD4+ memory/effector T cells. This signature consists of unique pathogenesis-associated epigenetic changes which extend beyond general T cell activation-induced alterations, indicating that disease-specific (super-)enhancers contribute to JIA pathogenesis. In addition, our analysis shows that there is a profound enrichment of JIA-related SNPs in (super-)enhancers in JIA patients compared to controls, illustrating the importance of these non-coding regions for disease pathogenesis. H3K27ac ChIP-sequencing of CD4+ memory/effector T cells derived from peripheral blood (PB) from healthy controls (HC) and PB or synovial fluid (SF) from JIA patients.
2015-09-15 | E-GEOD-71596 | biostudies-arrayexpress
Project description:Identify biomarkers to predict response to therapy in polyarticular juvenile idiopathic arthritis (JIA) using gene expression microarrays. 42 samples from 13 controls, 14 active patients, 9 patients in clinical remission with medication (CRM), and 6 patients in clinical remission without medication (CR). All patients had polyarticular JIA.
2009-04-13 | E-GEOD-15645 | biostudies-arrayexpress
Project description:Identify biomarkers to predict response to therapy in polyarticular juvenile idiopathic arthritis (JIA) using gene expression microarrays.
2009-04-13 | GSE15645 | GEO
Project description:With H3K27ac chromatin immunoprecipitation we identified a disease-specific, inflammation-associated, (super-)enhancer signature in JIA patient synovial fluid-derived CD4+ memory/effector T cells. This signature consists of unique pathogenesis-associated epigenetic changes which extend beyond general T cell activation-induced alterations, indicating that disease-specific (super-)enhancers contribute to JIA pathogenesis. In addition, our analysis shows that there is a profound enrichment of JIA-related SNPs in (super-)enhancers in JIA patients compared to controls, illustrating the importance of these non-coding regions for disease pathogenesis.
2015-09-15 | GSE71596 | GEO
Project description:Systemic-onset juvenile idiopathic arthritis (soJIA) is a rheumatic disease in childhood characterized by systemic symptoms and a relatively poor prognosis. The peripheral leukocytes are thought to play the pathological role of soJIA although the exact cause is still obscure. In this study, we aimed to clarify the cellular functional abnormality in those cells. Here, we analyzed the gene expression profile in peripheral leukocytes from 51 patients with soJIA, 6 patients with poly-articular type JIA (polyJIA) and 8 healthy children utilizing DNA microarrays. A total of 3,491 genes, including genes related to immune reponse and metabolism, were differentially expressed in patients with soJIA compared to healthy individuals. The result provides insight into the pathogenesis of soJIA. Keywords: disease state analysis Total RNA was extracted from peripheral leukocytes from 51 soJIA patients, 6 poly-articular type JIA patients, and 8 healthy children. The gene expression profile was analyzed with DNA microarrays.
2010-05-26 | E-GEOD-8361 | biostudies-arrayexpress
Project description:Juvenile idiopathic arthritis (JIA) is a chronic rheumatic disease with altered transcriptional signatures at the site of inflammation. mRNA transcription and translation are amongst other epigenetic mechanisms tightly regulated by specific miRNA expression. To determine the roles of different miRNAs within JIA pathogenesis we performed a global miRNA expression analysis in parallel in cells from the arthritic joint and peripheral blood of JIA patients, which demonstrates a different composition of miRNA expression at the site of inflammation. Bioinformatic analysis of predicted miRNA target genes suggests a huge overrepresentation of genes involved in metabolic and oxidative stress pathways in the inflamed joint. On the cellular level enhanced reactive oxygen species (ROS) and signs of highly activated metabolism in JIA T cells are present. Despite enhanced ROS levels within the local inflammatory milieu, JIA T cells are hyperproliferative and reveal a TNFa dependent overexpression of miR-23a, which is an inhibitor of PPIF, the regulator of mitochondrial ROS escape. TNFa blockade reduces miRNA-23a, rescues PPIF expression and ROS shuttling and thereby inhibits hyperproliferation. Our data show a novel mechanism of T cell proliferation and metabolism in JIA, which is mediated by miRNA dependent mitochondrial ROS shuttling.
2022-07-26 | GSE134984 | GEO