To determine whether IRF5 is only essential for FcγR-TLR cross-talk in moDCs, or whether it is also required for FcγR-TLR cross-talk in other cell types, we assessed the effect of IRF5 silencing on human macrophages, which are the main source of TNF in inflamed synovia of RA patients (23). This evidence concerns the gene FCGR2A and rheumatoid arthritis.