Interleukin-17A (IL-17A) is a proinflammatory cytokine that plays a critical role in host defense against systemic Candida albicans infection in mice. This study evaluated the role of murine IL-17A and its receptor (IL-17AR) in systemic candidiasis. IL-17AR knockout (IL-17AR^-/-^) mice showed significantly reduced survival and increased fungal burden in the kidneys compared to normal mice. These mice also exhibited impaired neutrophil mobilization and delayed influx into infected organs. In contrast, in vivo expression of mIL-17A protected normal mice from a lethal dose of C. albicans, suggesting that the mIL-17A/mIL-17AR system is essential for normal fungal host defense. IL-17A could serve as a potential therapeutic cytokine for systemic C. albicans infections in immunocompromised patients. Fungal infections remain a major cause of morbidity and mortality in immunocompromised individuals, particularly those undergoing cancer chemotherapy or HIV. Neutrophils are crucial for fungal host defense, and their dysfunction can lead to severe infections. IL-17A is primarily expressed in activated T cells and has been shown to stimulate granulopoiesis and neutrophil migration. In systemic candidiasis, Th1 responses improve survival, while Th2 responses are associated with worse outcomes. IL-17A does not fit into the Th1/Th2 model, suggesting it is an independent modulator of immune responses. The study used a murine model to investigate the role of IL-17A in systemic candidiasis. IL-17AR^-/-^ mice showed impaired neutrophil response and increased fungal burden, while in vivo expression of mIL-17A enhanced survival and reduced fungal growth. These findings suggest that IL-17A is essential for neutrophil mobilization and fungal host defense. However, other cytokines like G-CSF and GM-CSF also play roles in neutrophil activation and fungal defense. Despite this, IL-17A appears to be a distinct and necessary component of the immune response to fungal infections. The study highlights the importance of IL-17A in systemic fungal infections and suggests its potential as a therapeutic agent for immunocompromised patients. Further research is needed to fully understand the complex interactions between IL-17A and other immune components in fungal host defense.Interleukin-17A (IL-17A) is a proinflammatory cytokine that plays a critical role in host defense against systemic Candida albicans infection in mice. This study evaluated the role of murine IL-17A and its receptor (IL-17AR) in systemic candidiasis. IL-17AR knockout (IL-17AR^-/-^) mice showed significantly reduced survival and increased fungal burden in the kidneys compared to normal mice. These mice also exhibited impaired neutrophil mobilization and delayed influx into infected organs. In contrast, in vivo expression of mIL-17A protected normal mice from a lethal dose of C. albicans, suggesting that the mIL-17A/mIL-17AR system is essential for normal fungal host defense. IL-17A could serve as a potential therapeutic cytokine for systemic C. albicans infections in immunocompromised patients. Fungal infections remain a major cause of morbidity and mortality in immunocompromised individuals, particularly those undergoing cancer chemotherapy or HIV. Neutrophils are crucial for fungal host defense, and their dysfunction can lead to severe infections. IL-17A is primarily expressed in activated T cells and has been shown to stimulate granulopoiesis and neutrophil migration. In systemic candidiasis, Th1 responses improve survival, while Th2 responses are associated with worse outcomes. IL-17A does not fit into the Th1/Th2 model, suggesting it is an independent modulator of immune responses. The study used a murine model to investigate the role of IL-17A in systemic candidiasis. IL-17AR^-/-^ mice showed impaired neutrophil response and increased fungal burden, while in vivo expression of mIL-17A enhanced survival and reduced fungal growth. These findings suggest that IL-17A is essential for neutrophil mobilization and fungal host defense. However, other cytokines like G-CSF and GM-CSF also play roles in neutrophil activation and fungal defense. Despite this, IL-17A appears to be a distinct and necessary component of the immune response to fungal infections. The study highlights the importance of IL-17A in systemic fungal infections and suggests its potential as a therapeutic agent for immunocompromised patients. Further research is needed to fully understand the complex interactions between IL-17A and other immune components in fungal host defense.