The development of new treatments for rheumatoid arthritis (RA) is limited by our incomplete understanding of disease pathogenesis. Particularly, those pathways mediating disease onset, failed repair, and the development of treatment-refractory states are poorly understood. Myeloid cells (including dendritic cells, monocytes, macrophages) likely participate in such processes in RA. We recently discovered a novel epigenetic control mechanism of myeloid cells mediated via microRNA (miR) and obtained evidence for deregulation of this process in RA. We hypothesised that microRNAs controls transcriptional responses to growth and environmental factors of mononuclear myeloid cell subtypes and that its disregulation can contribute to the cause and perpetuation of arthritis.
Disclosure of Interest None declared