Here we combined gene expression and advanced bioinformatics analyses to demonstrate that (i) miR-223 is selectively upregulated in CD14+ cells from SF of RA patients with active disease; (ii) Notch activation represses miR-223 expression in myeloid cells; (iii) miR-223 targets ARNT, a necessary co-receptor for AHR-dependent transcriptional activity; (iv) miR-223 prevents AHR-mediated inhibition of pro-inflammatory cytokines; and (v) AHR target genes and ARNT protein itself are downmodulated in RA compared to OA synovial tissues. Here, CD14 is linked to rheumatoid arthritis.