Mice lacking IL-17A and IL-17F or components of the IL-17 receptor (Il17ra−/− and Il17rc−/− mice) display strongly increased fungal loads compared to control mice.34–40 The same also applies to mice that lack factors required for the development of IL-17 secreting cells (Rorc−/−, Il23p19−/−mice).34,37,40 In addition to T cells, innate lymphoid cells and γδ T cells have also been implicated in IL-17-dependent antifungal immunity in mice, in particular at the onset of infection,34,40–42 as most studies so far employed models of acute C. albicans infection. This evidence concerns the gene IL17A and infection.