The pathogenesis of IgG4-RD has been proposed that Tfh cells induce IgG4 class-switching and differentiation of plasmablasts and plasma cells [6, 32], and B cells and plasmablasts present disease-specific antigens and activate CD4+ CTLs, which drives the inflammatory and fibrotic processes [3–7, 32]. This evidence concerns the gene CD4 and immunoglobulin G4-related sclerosing disease.