The conceivable mechanisms of this phenomenon are: (1) an increased number of activated Tfh2 cells; (2) involvement of altered co-stimulatory molecules in the process of collaboration between Tfh2 cells and B cells [52]; (3) enhanced cytokine production, such as IL-4, IL-10, IL-13 and IL-21 from Tfh2 cells known for IgG4 class-switching [53]; and (4) an intrinsic alteration of naïve B cells in IgG4-RD patients. Here, IL10 is linked to immunoglobulin G4-related sclerosing disease.