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Abstract
Genetic and environmental factors contribute to the risk for rheumatoid arthritis (RA), with epigenetics serving as a possible interface through which risk factors contribute to RA. High-throughput technologies for interrogating genome and epigenome, and the availability of genetic and epigenetic datasets across a diversity of cell types, enable the identification of candidate causal genetic variants for RA to study their function in core RA processes. To date, RA risk variants were studied in the immune cells but not joint resident cells, for example, synovial fibroblasts. Synovial fibroblasts from different joints are distinct, anatomically specialized cells, defined by joint-specific transcriptomes, epigenomes and phenotypes. Cell type-specific analysis of epigenetic changes, together with genetic fine mapping and interrogation of chromatin 3D interactions may identify new disease relevant pathways, potential therapeutic targets and biomarkers for RA progression or therapy response.
Acknowledgements
The authors thank Caroline Ospelt for fruitful discussion.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.