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T cells are required for normal host defense against fungal infection, and individuals with T cell.deficiency syndromes are highly susceptible to fungal pathogens. Interleukin (IL)-17A is a proinflammatory cytokine that interconnects myeloid and lymphoid host defense. The role of murine (m) IL-17A/mIL-17A receptor (R) interactions was evaluated in a murine model of systemic candidiasis. In response to systemic challenge with Candida albicans, expression of mIL-17A was induced, and IL-17AR knockout (IL-17AR^−/−) mice had dosedependent, substantially reduced survival. Fungal burden in the kidneys of IL-17AR^−/− mice was dramatically increased (25-fold at 96 h). In IL-17AR^−/− mice, both mobilization of peripheral neutrophils and their influx to infected organs were significantly impaired and delayed. In vivo expression of mIL-17A protected normal mice from a lethal dose of C. albicans (100% at day 7 and …