IL1B and skin infection: Although Th17 development is severely impaired in IL-1R-deficient mice in vivo[61], [62] and γδ T cell production of IL-17 is enhanced in the presence of IL-1β [19], [63], the numbers and activity of Th17 and γδ T cells may increase during the course of the S. aureus skin infection and compensate for absence of IL-1β activity.