Immunity to infection in IL-17-deficient mice and humans.

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