In accordance with [10], we found that IL-23-deficient mice displayed highly increased fungal burden in the kidney, the major target organ of C. albicans in this model, 48h post infection compared to their wildtype counterparts (Fig 1A). Systemic C. albicans infection of Il23rgfp/gfp mice, which equal IL-23R-deficient mice if the IL-23R-GFP knock-in allele is bred to homozygosity [25], mirrored infection of IL-23 cytokine-deficient mice with a massively increased fungal burden compared to their WT counterparts (Fig 1A). Here, IL23A is linked to infection.