In a murine model of dermonecrosis, infection with an α-toxin-deficient S. aureus strain resulted in enhanced innate and adaptive immune responses, compared with infection with wild-type strain, as illustrated by increased neutrophil infiltration, influx of innate IL-17+ γδ T cells, recruitment of TH1 and TH17 cells, and enhanced pro-inflammatory cytokine and chemokine production. This evidence concerns the gene IL17A and infection.