Regarding the pathophysiology of IgG4-RD, the most widely accepted theory is that there is a relationship between environmental factors (e.g., infections with Helicobacter pylori, Mycobacterium tuberculosis and Gram-negative bacteria) and immunological factors (e.g., stimulation of Toll-like receptors) that trigger an immune response at the expense of Th-2 lymphocytes, with an increase in interleukins (IL) such as IL-4, IL-5 and IL-13. This evidence concerns the gene IL4 and infection.