We investigated the mechanism for development of dry eye disease in the Pinkie mouse strain with a loss of function RXRa mutation. Compared to wild type (WT) C57BL/6, Pinkie has increased signs of dry eye disease, including corneal barrier disruption, conjunctival cornification and goblet cell , and corneal vascularization, opacification, and ulceration with aging. Single cell RNA sequencing of conjunctival immune cells shows gd T cells are the predominant IL-17 expressing population in WT and Pinkie, with a greater percentage of gd T cells in Pinkie. There is significantly increased expression of IL-17a and IL-17f in conventional T cells and increased expression IL-17f in gd T cells in Pinkie compared to WT. The tear concentration of the IL-17 inducer IL-23 is significantly higher in Pinkie.  Flow cytometry and immunostaining reveals an increased number of IL-17+ gd T cells in the Pinkie conjunctiva. Treatment of gd T cells with the natural RXRa ligand 9-cis retinoic acid (RA) suppresses stimulated IL-17 production. Additionally,  treatment of monocytes with 9-cis RA in vitro suppresses the stimulatory activity of their supernatant on gd T cell IL-17 production. Compared to WT bone marrow chimeric mice, Pinkie bone marrow chimeras have increased IL-17+ gd T cells in the conjunctiva. Anti-IL-17 treatment suppresses desiccating stress induced corneal MMP-9 production and conjunctival goblet cell loss in Pinkie chimeras. These findings indicate that RXRa suppresses generation of dry eye disease inducing gd T17 cells in the conjunctiva and identifies RXRa as a potential therapeutic target in dry eye.