Mice with defective IL‐17 immunity display a broad vulnerability to various infectious agents at diverse mucocutaneous surfaces. In humans, the study of patients with various primary immunodeficiencies, including autosomal dominant hyper‐IgE syndrome caused by dominant‐negative STAT3 mutations and autosomal recessive autoimmune polyendocrinopathy syndrome type 1 caused by null mutations in AIRE, has suggested that IL‐17A, IL‐17F and/or IL‐22 are essential for mucocutaneous immunity to Candida albicans. This hypothesis was confirmed by the identification of rare patients with chronic mucocutaneous candidiasis (CMC) due to autosomal recessive IL‐17RA deficiency and autosomal dominant IL‐17F deficiency. Heterozygosity for gain‐of‐function mutations in STAT1 in additional patients with CMC was recently shown to inhibit the development of IL‐17 T cells. Although the infectious phenotype of patients with CMC and inborn errors of IL‐17 immunity remains to be finely delineated, it appears that human IL‐17A and IL‐17F display redundancy for protective immunity in natural conditions that is not seen in their mouse orthologs in experimental conditions.