To define the factors that shape disease-associated macrophage states in affected tissues, we generated human blood-derived macrophages from four donors and activated them with eight defined mixtures of inflammatory factors, focusing particularly on the effects of antiviral interferons (IFN-β and IFN-γ) and pro-inflammatory cytokines such as TNF that mediate CRS and tissue pathology in RA and IBD [40] (Fig. 3a, Additional file 2: Figure S7a, “Methods”). This evidence concerns the gene IFNB1 and congenital rubella syndrome.