IGHE and infection: It is currently believed that abnormal immune response against infection, allergen, or tissue injury may be the initiating factors in the pathogenesis of IgG4-RD, and then triggers can activate T follicular helper (Tfh) and T follicular regulatory (Tfr) cell immune response, and the subsequent production of IL-4/IL-10 cytokines can promote the production and class switch of IgG4 and IgE in plasmablasts, eosinophil recruitment, and fibroblast activation [2, 30, 31] Finally, it leads to the onset of IgG4-RD.