Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Immunol. 2010 Aug;22(4):467-74. doi: 10.1016/j.coi.2010.06.009. Epub 2010 Jul 30.

Inborn errors of mucocutaneous immunity to Candida albicans in humans: a role for IL-17 cytokines?

Author information

  • 1Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Inserm U980, University Paris Descartes, Necker Medical School, Paris, France, EU. anne.puel@inserm.fr

Abstract

The various clinical manifestations of chronic mucocutaneous candidiasis (CMC) often result from acquired T-cell immunodeficiencies. More rarely, CMC results from inborn errors of immunity, the recent dissection of which has shed light on the molecular mechanisms of mucocutaneous immunity to Candida albicans. CMC may accompany various other infectious diseases in patients with almost any broad and profound T-cell primary immunodeficiency. By contrast, CMC is one of the few key infections in patients with autosomal dominant hyper IgE syndrome (mutations in STAT3), and in rare patients with autosomal recessive predisposition to mucocutaneous and invasive fungal infections (mutation in CARD9). In patients with mutations in STAT3 and CARD9, the development of IL-17-producing T cells is impaired. Moreover, CMC is the principal, if not only, infection in patients with autosomal recessive autoimmune polyendocrinopathy syndrome-I (mutations in AIRE). Patients with this condition have high titers of neutralizing autoantibodies (auto-Abs) against the IL-17 cytokines IL-17A, IL-17F, and IL-22. Collectively, these data suggest that human IL-17A, IL-17F, and IL-22 are essential for mucocutaneous immunity to C. albicans. They also suggest that the distinct syndrome of isolated CMC, without auto-immunity or other infections, may be caused by inborn errors of IL-17 immunity.

Copyright 2010 Elsevier Ltd. All rights reserved.

PMID:
20674321
[PubMed - indexed for MEDLINE]
PMCID:
PMC3770911
Free PMC Article

Images from this publication.See all images (1)Free text

Figure 1
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk