Through the help of RNA-seq technology, their data demonstrate that choroidal γδ T cells are activated by RPE injury in response to NaIO3 treatment, and that they express genes that encode immunosuppressive cytokines, such as IL-4 and IL-10. γδ T cell–deficient mice developed profound RPE and retinal damage at doses that caused minimal effects in wild-type mice, and adoptive transfer of γδ T cells prevented sensitization. Intravitreal injection of IL-4 and IL-10 ameliorated RPE toxicity that was shown to be induced by NaIO3. Ex vivo coculture of γδ T cells with RPE explants activated the production of anti-inflammatory cytokines via an aryl hydrocarbon receptor (AhR)–dependent mechanism. AhR deficiency abolished the protective effects of γδ T cells after adoptive transfer.
Collectively, these findings define important roles for choroid γδ T cells in maintaining tissue homeostasis in the outer retina.