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. 2019 Jul 13;5(7):634–638. doi: 10.1016/j.jdcr.2019.05.018

Fig 4.

Fig 4

Parallels and intersection of UC and IgG4-related disease pathways. A, An unknown antigen in the IgG4 pathway and an epithelial autoantigen in the UC pathway both stimulate antigen-presenting cells. B, Antigen-presenting cells activate naïve T cells and lead to a Th2-dominant response, with increases in the number of Tregs and Th17 cells. C, Th2 cells release IL-4, which promotes naïve B-cell differentiation into plasma cells and immunoglobulin isotype switching to IgG4. D, IgG4 infiltration of orbits leads to fibrosis and IgG4-ROD. E, Tregs release IL-10 and transforming growth factor-β, which contribute to fibrosis. F, Th17 cells and Th17-related cytokines induce autoimmunity and promote inflammation.