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RNA-sequencing of cells derived from the site of inflammation of Juvenile Idiopathic Arthritis patients

ABSTRACT: Through RNA sequencing of CD4+ Tmemory/effector cells derived from the synovium of JIA patients and healthy controls, we analyzed the JIA gene expression signature. Treatment of autoinflammatory site-derived patient T cells with the BET-inhibitor JQ1 inhibited immune-related super-enhancers and preferentially reduced disease-associated gene expression, including cytokine-related processes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71595 | GEO | 2015/09/15

SECONDARY ACCESSION(S): PRJNA291597

REPOSITORIES: GEO

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RNA-sequencing of cells derived from the site of inflammation of Juvenile Idiopathic Arthritis patients

Project description:Through RNA sequencing of CD4+ Tmemory/effector cells derived from the synovium of JIA patients and healthy controls, we analyzed the JIA gene expression signature. Treatment of autoinflammatory site-derived patient T cells with the BET-inhibitor JQ1 inhibited immune-related super-enhancers and preferentially reduced disease-associated gene expression, including cytokine-related processes. RNA-sequencing of CD4+ memory/effector T cells derived from Healthy Controls (HC) and JIA patients upon JQ1 treatment.

2015-09-15 | E-GEOD-71595 | biostudies-arrayexpress

Juvenile idiopathic arthritis: peripheral blood cells

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.

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2009-04-13 | E-GEOD-15645 | biostudies-arrayexpress

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Epigenetic profiling of Juvenile Idiopathic Arthritits (JIA) patients

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

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2015-09-15 | GSE71596 | GEO

Gene expression predictors of extension in oligoarticular juvenile idiopathic arthritis (JIA)

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miR-23a regulates T cellular Redox metabolism in juvenile idiopathic arthritis

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

Common Immunologic Pathways Between Oligoarticular and Polyarticular Juvenile Idiopathic Arthritis

Project description:The polyarticular and oligoarticular forms of juvenile idiopathic arthritis are classified as distinct entities. At the same time, many children who present with an oligoarticular phenotype eventually evolve to a polyarticular disease pattern, suggesting that the phenotypes might share with overlapping molecular mechanisms. Using gene expression microarrays, we found that 14 genes in neutrophils and 55 genes in PBMC shows common patterns of differential expression when children with active oligoarticular and polyarticular JIA were compared with healthy controls. These results demonstrate that there are commonalities between oligoarticular and polyarticular JIA that suggest overlapping immune mechanisms. Total RNA was extracted from isolated PBMC and neutrophils from 14 patients with polyarticular JIA and 8 patients with pauciarticular JIA. Total RNA was extracted from neutrophils from 13 healthy controls and from PBMC from 15 healthy controls. Insufficient RNA for microarrays was obtained from neutrophils from two of the healthy controls.

2015-04-07 | E-GEOD-67596 | biostudies-arrayexpress

ChIP-seq in neutrophils from Juvenile Idiopathic Arthritis

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