Fig. 1

The mechanisms of autoimmune dacryoadenitis and MSC treatment for it. Both the innate and adaptive immune systems participate in the pathogenesis of autoimmune dacryoadenitis, which occurs when the ocular surface is stimulated by various factors. Cytokines such as IL-6, IL-1, and TNF-α have been suggested to play a role in the destruction of acinar cells. The proinflammatory milieu promotes the activation and maturation of APCs, which contribute to the induction of Th1 cells and Th17 cells. IFN-γ and IL-17, separately secreted by Th1 and Th17 cells, promote the production of proinflammatory cytokines/chemokines which induce ocular surface inflammation. MSCs protect the ocular surface by inhibiting the infiltration of inflammatory cells, restoring Th1/Th2 homeostasis, suppressing Th17 cells, activating Tregs, stimulating epithelial cells, and promoting goblet cell regeneration. They inhibit the activation and proliferation of T cells and favor the differentiation of T cells into Th2 cells, thus restoring Th1/Th2 homeostasis. Furthermore, MSCs could exert their protective effects by activating Tregs and suppressing Th17 cells. In addition, MSCs promote tissue repair by stimulating epithelial cell and goblet cell regeneration