TLR3 and immunoglobulin G4-related sclerosing disease: Based on these observations, we speculate that human AIP/IgG4-RD is initiated by a similar TLR3-bearing cDC-dependent IFN-α/β–inducing mechanism, but in this case the TLR3 stimulus might consist of an organism in the gut microflora (or a product derived from the microflora) that gains access to the pancreas and/or another secretory organ (27).