This study describes an essential role for interleukin-17 (IL-17)-secreting innate lymphoid cells (ILCs) in promoting protective immunity to an oral fungal infection. In mice infected sublingually with Candida albicans, the adaptive immune system was shown to be dispensable for the resolution of infection. Both MHC class II-deficient mice and Rag1−/− mice could control this infection. Furthermore, mice lacking γδ T cells or natural killer T cells could also clear the infection. By contrast, Rag1−/− mice that were treated with CD90-specific antibodies to deplete ILCs could not recover following C. albicans infection. Depletion of ILCs led to a marked reduction in the early induction of IL-17A and IL-17F in the tongues of C. albicans-infected mice. The authors suggest that ILCs mediate protection by upregulating IL-17 in response to IL-23 that is generated early following infection with C. albicans.