Candida albicans (C. albicans) is a opportunistic fungus which causes a wide spectrum of infections from mild to severe and often lethal disease in the setting of immunosuppression. Defense against C. albicans is largely depends on C-type lectin receptors (CLRs) as well as IL-17 family cytokines. Here, we developed epicutaneous candidiasis (ECC) mouse model, in which C. albicans was inoculated occlusively on shaved skin. In this model, skin inflammation reached a peak on day 2 with neutrophil infiltration and subsided by day 7 in WT, Il17a -/- and Il17f -/- mice, while Il17a -/--Il17f -/- mice showed more severe inflamed skin even on day 7 with the high fungal burden, indicating the importance of IL-17 for ECC defense. However, fungal recognition receptors TLR2, Dectin-1, Dectin-2, and the adaptor signaling molecules MyD88, FcRγ, and Card9 were dispensable for clearance of C. albicans in the skin. In addition, we detected lower mRNA expression of antimicrobial peptides (AMPs) and less number of neutrophils in the infected skin from Il17a -/--Il17f -/- mice than in that of WT mice. Neutrophils isolated from Il17a -/--Il17f -/- mice had less killing activity against C. albicans than those from WT mice in vitro. These findings indicate that IL-17 plays a pivotal role in cutaneous host defense by recruiting and activating neutrophils to eradicate C. albicans in the epidermis.