After corneal epithelial abrasion, leukocytes and platelets rapidly enter the corneal stroma, and CCR6+ IL-17+ γδ T cells migrate into the epithelium. γδ T-cell-deficient (TCRδ−/−) mice have significantly reduced inflammation and epithelial wound healing. Epithelial CCL20 mRNA increased 19-fold at 3 h, and protein increased∼ 16-fold at 6 h after injury. Systemic or topical treatment of wild-type C57BL/6 mice with anti-CCL20 reduced γδ T-cell accumulation in the cornea by> 50% with a concomitant decrease in epithelial healing and stromal inflammation. In addition to CCR6 and IL-17, corneal γδ T cells stained positively for RORγt, IL-23R, and IL-22. Anti-IL-22 reduced peak cell division of the healing epithelium by 52%. Treatment of TCRδ−/− mice with rIL-22 significantly promoted wound closure, with peak epithelial cell division increased> 3-fold. In addition, rIL-22 restored neutrophil and platelet influx in the TCRδ−/− mice to wild-type levels and increased CXCL1 production by wounded corneal explants> 2-fold. These results indicate that an important aspect of the healing response to corneal epithelial abrasion includes CCL20-dependent influx of CCR6+ IL-17+ IL-22+ γδ T cells and that IL-22 contributes to the inflammatory response and promotes epithelial healing.—Li, Z., Burns, AR, Byeseda Miller, S., Smith, CW CCL20, γδ T cells, and IL-22 in corneal epithelial healing.