Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 9, Pages 2246-2254Publisher
WILEY
DOI: 10.1002/eji.201242605
Keywords
Cytokines; IL-17; Infectious diseases
Categories
Funding
- INSERM
- University Paris Descartes
- National Center for Research Resources
- National Center for Advancing Sciences (NCATS)
- National Institutes of Health [8UL1TR000043]
- ANR [GENCMCD 11-BSV3-005-01]
- St. Giles Foundation
- Candidoser Association
- TAMOP [4.2.1./B-09/1/KONV-2010-0007]
- AXA Research Fund
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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.
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