ArticleJCI insight2018
Identification of enhanced IFN-γ signaling in polyarticular juvenile idiopathic arthritis with mass cytometry.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Functional and computational interrogation of juvenile idiopathic arthritis risk loci in CD4+ T cells.HGG advances · 2026Article
- Interferon-Driven Tryptophan Metabolism Links Inflammation and Mental Health in Juvenile Dermatomyositis.Inflammation · 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
- Transcriptional Profiling of Tofacitinib Treatment in Juvenile Idiopathic Arthritis: Implications for Treatment Response Prediction.Arthritis care & research · 2025Article
- Inflammation-profiling reveals activated pathways and biomarkers with predictive potential in oligoarticular juvenile idiopathic arthritis.Frontiers in immunology · 2025Article
- A systematic strategy for identifying causal single nucleotide polymorphisms and their target genes on Juvenile arthritis risk haplotypes.BMC medical genomics · 2024Article
- Th17/1 and ex-Th17 cells are detected in patients with polyarticular juvenile arthritis and increase following treatment.Pediatric rheumatology online journal · 2024Article
- Transcriptomic signatures of classical monocytes reveal pro-inflammatory modules and heterogeneity in polyarticular juvenile idiopathic arthritis.Frontiers in immunology · 2024Article
- Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition.Rheumatology (Oxford, England) · 2023Article
- Immunomics analysis of rheumatoid arthritis identified precursor dendritic cells as a key cell subset of treatment resistance.Annals of the rheumatic diseases · 2023Article
- Analysis of chromatin data supports a role for CD14+ monocytes/macrophages in mediating genetic risk for juvenile idiopathic arthritis.Frontiers in immunology · 2022Article
- Increased Development of Th1, Th17, and Th1.17 Cells Under T1 Polarizing Conditions in Juvenile Idiopathic Arthritis.Frontiers in immunology · 2022Article
- Signals and Mechanisms Regulating Monocyte and Macrophage Activation in the Pathogenesis of Juvenile Idiopathic Arthritis.International journal of molecular sciences · 2021Review
- Seroprevalence of Antibodies against SARS-CoV-2 in Children with Juvenile Idiopathic Arthritis a Case-Control Study.Journal of clinical medicine · 2021Article
- CD4+ T cells from children with active juvenile idiopathic arthritis show altered chromatin features associated with transcriptional abnormalities.Scientific reports · 2021Article
- Differential Accumulation and Activation of Monocyte and Dendritic Cell Subsets in Inflamed Synovial Fluid Discriminates Between Juvenile Idiopathic Arthritis and Septic Arthritis.Frontiers in immunology · 2020Article
- Immunomics in Pediatric Rheumatic Diseases.Frontiers in medicine · 2019Review
- Using Chromatin Architecture to Understand the Genetics and Transcriptomics of Juvenile Idiopathic Arthritis.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Polyarticular juvenile idiopathic arthritis (JIA) is among the most challenging of the JIA subtypes to treat. Even with current biologic therapies, the disease remains difficult to control in a substantial subset of patients, highlighting the need for new therapies. The aim of this study was to use the high dimensionality afforded by mass cytometry with phospho-specific antibodies to delineate signaling abnormalities in immune cells from treatment-naive polyarticular JIA patients. Peripheral blood mononuclear cells were isolated from 17 treatment-naive polyarticular JIA patients, 10 of the patients after achieving clinical remission, and 19 healthy controls. Samples were stimulated for 15 minutes with IL-6 or IFN-γ and analyzed by mass cytometry. Following IFN-γ stimulation, increased STAT1 and/or STAT3 phosphorylation was observed in subsets of CD4 T cells and classical monocytes from treatment-naive patients. The enhanced IFN-γ signaling was associated with increased expression of JAK1 and SOCS1 in CD4 T cells. Furthermore, substantial heterogeneity in surface marker expression was observed among the subsets of CD4 T cells and classical monocytes with increased IFN-γ responsiveness. The identification of enhanced IFN-γ signaling in CD4 T cells and classical monocytes from treatment-naive polyarticular JIA patients provides mechanistic support for investigations into therapies that attenuate IFN-γ signaling in this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.