In IgG4-related disease, TLR7+ CD163+ M2 Mφs directly drive fibrosis by secreting TGF-β and other profibrotic factors via the TLR7/IRAK4/NF-κB pathway (Figure 3B) (56). This evidence concerns the gene TGFB1 and immunoglobulin G4-related sclerosing disease.