To assess the role of IL-22 and IDO1 in murine VVC, we intravaginally infected C57BL/6, IL-22- or IDO1-deficient mice with Candida blastospores and evaluated resistance to infection in terms of vaginal histopathology, PMN recruitment in vaginal lavages, expression of chemotactic S100A8 and S100A9 proteins, known to mediate PMN migration in murine VVC [8] and local fungal growth. This evidence concerns the gene S100A9 and infection.