ArticleRheumatology (Oxford, England)2023
Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition.
Article in Rheumatology (Oxford, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Synovial fluid potentiates local fibroblasts to drive monocyte activation in juvenile idiopathic arthritis.Arthritis research & therapy · 2026Article
- Dysregulation of YTHDF2 promotes the over expression of interferon beta in anti-MDA5 antibody-positive dermatomyositis.Arthritis research & therapy · 2026Article
- Dynamic Balance of Histone H3 Methylation: Regulatory Mechanisms and Therapeutic Prospects in RA Immune Dysregulation and Bone Metabolism Imbalance.Journal of immunology research · 2026Review
- Reduced Expression of mInternational journal of molecular sciences · 2025Article
- Oleanane triterpenoids with C-14 carboxyl group fromFrontiers in pharmacology · 2024Article
- The clinical and experimental treatment of Juvenile Idiopathic Arthritis.Clinical and experimental immunology · 2023Review
- Triterpenoid and Coumarin Isolated fromMolecules (Basel, Switzerland) · 2023Article
- Synovial monocytes contribute to chronic inflammation in childhood-onset arthritis via IL-6/STAT signalling and cell-cell interactions.Frontiers in immunology · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesHow the local inflammatory environment regulates epigenetic changes in the context of inflammatory arthritis remains unclear. Here we assessed the transcriptional and active enhancer profile of monocytes derived from the inflamed joints of JIA patients, a model well-suited for studying inflammatory arthritis.
methodsRNA sequencing and H3K27me3 chromatin immunoprecipitation sequencing (ChIP-seq) were used to analyse the transcriptional and epigenetic profile, respectively, of JIA synovial fluid-derived monocytes.
resultsSynovial-derived monocytes display an activated phenotype, which is regulated on the epigenetic level. IFN signalling-associated genes are increased and epigenetically altered in synovial monocytes, indicating a driving role for IFN in establishing the local inflammatory phenotype. Treatment of synovial monocytes with the Janus-associated kinase (JAK) inhibitor ruxolitinib, which inhibits IFN signalling, transformed the activated enhancer landscape and reduced disease-associated gene expression, thereby inhibiting the inflammatory phenotype.
conclusionThis study provides novel insights into epigenetic regulation of inflammatory arthritis patient-derived monocytes and highlights the therapeutic potential of epigenetic modulation for the treatment of inflammatory rheumatic diseases.
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