ArticleArthritis & rheumatology (Hoboken, N.J.)2015
Disease-Associated Single-Nucleotide Polymorphisms From Noncoding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Whole blood expression profiling from the TREAT trial: insights for the pathogenesis of polyarticular juvenile idiopathic arthritis.Arthritis research & therapy · 2016Trial
- 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
- Integrating Machine Learning and Multi-Omics to Explore Neutrophil Heterogeneity.Biomedicines · 2025Review
- 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
- A systematic strategy for identifying causal single nucleotide polymorphisms and their target genes on Juvenile arthritis risk haplotypes.BMC medical genomics · 2024Article
- The clinical and experimental treatment of Juvenile Idiopathic Arthritis.Clinical and experimental immunology · 2023Review
- Super-enhancer-associated gene CAPG promotes AML progression.Communications biology · 2023Article
- Semantic and Population Analysis of the Genetic Targets Related to COVID-19 and Its Association with Genes and Diseases.Advances in experimental medicine and biology · 2023Article
- A curious case of cyclin-dependent kinases in neutrophils.Journal of leukocyte biology · 2022Review
- Analysis of chromatin data supports a role for CD14+ monocytes/macrophages in mediating genetic risk for juvenile idiopathic arthritis.Frontiers in immunology · 2022Article
- Broadening our understanding of genetic risk for scleroderma/systemic sclerosis by querying the chromatin architecture surrounding the risk haplotypes.BMC medical genomics · 2021Article
- CD4+ T cells from children with active juvenile idiopathic arthritis show altered chromatin features associated with transcriptional abnormalities.Scientific reports · 2021Article
- Variant to Gene Mapping to Discover New Targets for Immune Tolerance.Frontiers in immunology · 2021Article
- Review
- Comprehensive functional annotation of susceptibility variants associated with asthma.Human genetics · 2020Article
- Article
- Immunome perturbation is present in patients with juvenile idiopathic arthritis who are in remission and will relapse upon anti-TNFα withdrawal.Annals of the rheumatic diseases · 2019Article
- Epigenetic landscapes suggest that genetic risk for intracranial aneurysm operates on the endothelium.BMC medical genomics · 2019Article
- Implications of juvenile idiopathic arthritis genetic risk variants for disease pathogenesis and classification.Current opinion in rheumatology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveJuvenile idiopathic arthritis (JIA) is considered a complex disease in which the environment interacts with inherited genes to produce a phenotype that shows broad interindividual variability. Twenty-four regions of genetic risk for JIA were identified in a recent genome-wide association study (GWAS); however, as is typical of the results of GWAS, most of the regions of genetic risk (22 of 24) were in noncoding regions of the genome. This study was undertaken to identify functional elements (other than genes) that might be located within the regions of genetic risk.
methodsWe used paired-end RNA sequencing to identify noncoding RNAs (ncRNAs) located within 5 kb of disease-associated single-nucleotide polymorphisms (SNPs). In addition, we used chromatin immunoprecipitation (ChIP) followed by sequencing to identify epigenetic marks associated with enhancer function (H3K4me1 and H3K27ac) in human neutrophils to determine whether enhancer-associated histone marks were enriched in the linkage disequilibrium blocks that encompassed the 22 SNPs identified in the GWAS.
resultsIn human neutrophils, we identified H3K4me1 and/or H3K27ac marks in 15 of the 22 regions previously identified as risk loci for JIA. In CD4+ T cells, 18 regions had H3K4me1 and/or H3K27ac marks. In addition, we identified ncRNA transcripts at the rs4705862 and rs6894249 loci in human neutrophils.
conclusionMuch of the genetic risk for JIA lies within or adjacent to regions of neutrophil and CD4+ T cell genomes that carry epigenetic marks associated with enhancer function and/or ncRNA transcripts. These findings are consistent with the hypothesis that JIA is fundamentally a disorder of gene regulation that includes both the innate and the adaptive immune system. Elucidating the specific roles of these noncoding elements within leukocyte genomes will be critical to our understanding of JIA pathogenesis.
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