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

Lookup NU author(s): Dr Desa Lilic



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. © 2010 Elsevier Ltd.

Publication metadata

Author(s): Puel A, Picard C, Cypowyj S, Lilic D, Abel L, Casanova J

Publication type: Review

Publication status: Published

Journal: Current Opinion in Immunology

Year: 2010

Volume: 22

Issue: 4

Pages: 467-474

Print publication date: 30/07/2010

ISSN (print): 0952-7915

ISSN (electronic): 1879-0372


DOI: 10.1016/j.coi.2010.06.009

PubMed id: 20674321