In this mouse model of S. aureus skin infection, neutrophil recruitment to the infection sites was dependent on epidermal γδ-T-cell production of IL-17 and this IL-17 induction is controlled by signals from IL-1, TLR2, and IL-23 as IL-17 production upon S. aureus infection is diminished in the Il1r1−/−, Tlr2−/−, and Il23a−/− mice but not Il12a−/− mice. This evidence concerns the gene IL23A and skin infection.