In addition, IL-17 has also been shown to be critical in promoting neutrophil recruitment and antimicrobial responses against S. aureus in various mouse models of infection (cutaneous infection, systemic infections, pneumonia and brain abscesses [52]–[56]) as well as in humans with hyper-IgE syndrome or with a deficiency in IL-17F or IL-17RA [50], [57]–[60]. This evidence concerns the gene IL17F and infection.