Gamma delta T cells play a pathogenic role in dry eye disease. Desiccating stress activates and recruits gamma delta (\gamma\delta) T cells by monocytes and natural killer (NK) cells. A pathway where desiccating stress directly stimulates \gamma\delta T cells is possible. 9-cis retinoic acid (RA) directly inhibits the \gamma\delta T cells and also acts on monocytes to indirectly inhibit the \gamma\delta T cells. \gamma\delta T cells contribute to dry eye disease (DED) pathogenesis through the secretion of IL-17 and IFN-\gamma. IL-17A upregulates MMP3 and MMP9 expression of corneal epithelial cells, mediating corneal epithelial barrier disruption. IL-17A activates cornified envelope precursor genes Sprr2g and Sprr2h resulting in corneal and conjunctival epithelial keratinization. IL-17A directly acts on corneal epithelial cells to promote VEGF-D secretion. The VEGF-D binds to VEGFR3 on the surface of lymphatic endothelial cells to cause lymphangiogenesis. IL-17A also indirectly acts on corneal epithelial cells through IL-1\beta to mediate the secretion of VEGF-A and VEGF-C to cause neovascularization. IL-17A promotes the secretion of pro-inflammatory cytokines IL-1\beta, IL-6, and TNF-\alpha by corneal and conjunctival epithelial cells. IL-6 induces the development of Th17 cells from naïve T cells. IL-1, TNF-\alpha, and IL-17A further promote the synthesis and secretion of CCL20 by corneal epithelial cells and stromal cells. CCL20 acts on the CD4+ T cells in draining lymph nodes and then exerts a strong chemotactic effect. CD4+T cells continue to secrete a variety of pro-inflammatory factors including IL-17A after reaching the ocular surface, promoting ocular surface inflammation. IFN-\gamma plays a complex role in DED, including the maturation of antigen-presenting cells (APCs), activation and recruitment of CD4+ T cells, thereby promoting epithelial keratinization and goblet apoptosis (Created with BioRender.com). TNF-\alpha, tumor necrosis factor-\alpha; IL-17, interleukin-17; IFN-\gamma, interferon-\gamma; VEGFR3, vascular endothelial growth factor receptor 3; MMP, matrix metalloproteinase; Th17, T helper 17; CCL20, C-C motif chemokine ligand 20.