Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by Janus-associated kinase (JAK) inhibition
Authors' conclusion
This study provides novel insights into epigenetic regulation of inflammatory arthritis patient-derived monocytes
Study context
- Population
- Monocytes derived from the inflamed joints of JIA patients
- Comparison
- JIA synovial fluid-derived monocytes, with and without ruxolitinib (JAKi) treatment
- Outcome
- Transcriptional and active enhancer profile of JIA synovial fluid-derived monocytes
Methodological detailsRNA sequencing, H3K27me3 chromatin immunoprecipitation sequencing (ChIP-seq)
- RNA sequencing
- H3K27me3 ChIP-seq
Main finding
As reported in the abstract
- Synovial-derived monocytes display an activated phenotype, regulated on the epigenetic level
- IFN signalling-associated genes increased and epigenetically altered in synovial monocytes
- Ruxolitinib (JAKi, inhibits IFN signalling) transformed the activated enhancer landscape and reduced disease-associated gene expression
Original publication
Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition. Rheumatology (Oxford). Published 10 January 2023. doi:10.
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