ArticleScientific reports2021
CD4+ T cells from children with active juvenile idiopathic arthritis show altered chromatin features associated with transcriptional abnormalities.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Differential transcriptional and epigenetic signatures in CD4Journal of translational autoimmunity · 2026Article
- Efforts towards a precision medicine approach in juvenile idiopathic arthritis.Rheumatology (Oxford, England) · 2026Review
- Functional and computational interrogation of juvenile idiopathic arthritis risk loci in CD4+ T cells.HGG advances · 2026Article
- Functional and Computational Interrogation of the Juvenile Idiopathic Arthritis Risk Loci Identifies Candidate Causal SNPs and Target Genes in CD4+ T cells.medRxiv : the preprint server for health sciences · 2025Article
- Defining three dimensional chromatin structures of pediatric and adolescent B cells using primary B cell and EBV-immortalized B cell reference genomes.BMC medical genomics · 2025Article
- Using genetics, genomics, and transcriptomics to identify therapeutic targets in juvenile idiopathic arthritis.HGG advances · 2025Article
- Systematic decoding of cis gene regulation defines context-dependent control of the multi-gene costimulatory receptor locus in human T cells.Nature genetics · 2024Article
- Identification of Mechanisms by Which Genetic Susceptibility Loci Influence Systemic Sclerosis Risk Using Functional Genomics in Primary T Cells and Monocytes.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Integrative multi-omics approaches to explore immune cell functions: Challenges and opportunities.iScience · 2023Review
- Cohesin-Mediated Chromatin Interactions and Autoimmunity.Frontiers in immunology · 2022Review
- Broadening our understanding of genetic risk for scleroderma/systemic sclerosis by querying the chromatin architecture surrounding the risk haplotypes.BMC medical genomics · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Juvenile idiopathic arthritis (JIA) is one of the most common chronic diseases in children. While clinical outcomes for patients with juvenile JIA have improved, the underlying biology of the disease and mechanisms underlying therapeutic response/non-response are poorly understood. We have shown that active JIA is associated with distinct transcriptional abnormalities, and that the attainment of remission is associated with reorganization of transcriptional networks. In this study, we used a multi-omics approach to identify mechanisms driving the transcriptional abnormalities in peripheral blood CD4+ T cells of children with active JIA. We demonstrate that active JIA is associated with alterations in CD4+ T cell chromatin, as assessed by ATACseq studies. However, 3D chromatin architecture, assessed by HiChIP and simultaneous mapping of CTCF anchors of chromatin loops, reveals that normal 3D chromatin architecture is largely preserved. Overlapping CTCF binding, ATACseq, and RNAseq data with known JIA genetic risk loci demonstrated the presence of genetic influences on the observed transcriptional abnormalities and identified candidate target genes. These studies demonstrate the utility of multi-omics approaches for unraveling important questions regarding the pathobiology of autoimmune diseases.
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