Upon binding to cell surface or intracellular receptors of Th17 cells, γδT cells, ILC3, mast cells, and other cells, IL-23 activates the Jak2-STAT3 intracellular signaling pathway, inducing effector cells such as Th17 to produce pro-inflammatory cytokines like IL-17 and IL-22, while also disrupting the barrier function of retinal pigment epithelial cells, thereby promoting the occurrence and progression of uveitis (80),Therefore, modulating the activity of the IL-23/IL-17 immunological axis may offer a potential therapeutic strategy for the treatment of SpA-associated uveitis. This evidence concerns the gene IL22 and uveitis.