The study investigates the role of interleukin-17A (IL-17A) in systemic anti-*Candida albicans* host defense in mice. IL-17A is a proinflammatory cytokine that connects myeloid and lymphoid host defense. In a murine model of systemic candidiasis, IL-17A expression was induced upon systemic challenge with *C. albicans*, and IL-17AR knockout (IL-17AR−/−) mice showed dose-dependent, significantly reduced survival. Fungal burden in the kidneys of IL-17AR−/− mice was dramatically increased, and both the mobilization of peripheral neutrophils and their influx to infected organs were impaired and delayed. In vivo expression of IL-17A protected normal mice from a lethal dose of *C. albicans*. The data suggest that the mIL-17A/mIL-17AR system is essential for normal fungal host defense in vivo, and IL-17A could be a potential therapeutic cytokine for systemic *C. albicans* infections in immunocompromised patients.The study investigates the role of interleukin-17A (IL-17A) in systemic anti-*Candida albicans* host defense in mice. IL-17A is a proinflammatory cytokine that connects myeloid and lymphoid host defense. In a murine model of systemic candidiasis, IL-17A expression was induced upon systemic challenge with *C. albicans*, and IL-17AR knockout (IL-17AR−/−) mice showed dose-dependent, significantly reduced survival. Fungal burden in the kidneys of IL-17AR−/− mice was dramatically increased, and both the mobilization of peripheral neutrophils and their influx to infected organs were impaired and delayed. In vivo expression of IL-17A protected normal mice from a lethal dose of *C. albicans*. The data suggest that the mIL-17A/mIL-17AR system is essential for normal fungal host defense in vivo, and IL-17A could be a potential therapeutic cytokine for systemic *C. albicans* infections in immunocompromised patients.