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Human dectin-1 deficiency and mucocutaneous fungal infections.

Ferwerda, Bart; Ferwerda, Gerben; Plantinga, Theo S; Willment, Janet A; van Spriel, Annemiek B; Venselaar, Hanka; Elbers, Clara C; Johnson, Melissa D; Cambi, Alessandra; Huysamen, Cristal; Jacobs, Liesbeth; Jansen, Trees; Verheijen, Karlijn; Masthoff, Laury; Morré, Servaas A; Vriend, Gert; Williams, David L; Perfect, John R; Joosten, Leo A B; Wijmenga, Cisca; van der Meer, Jos W M; Adema, Gosse J; Kullberg, Bart Jan; Brown, Gordon D; Netea, Mihai G.
N Engl J Med; 361(18): 1760-7, 2009 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-19864674
Mucocutaneous fungal infections are typically found in patients who have no known immune defects. We describe a family in which four women who were affected by either recurrent vulvovaginal candidiasis or onychomycosis had the early-stop-codon mutation Tyr238X in the beta-glucan receptor dectin-1. The mutated form of dectin-1 was poorly expressed, did not mediate beta-glucan binding, and led to defective production of cytokines (interleukin-17, tumor necrosis factor, and interleukin-6) after stimulation with beta-glucan or Candida albicans. In contrast, fungal phagocytosis and fungal killing were normal in the patients, explaining why dectin-1 deficiency was not associated with invasive fungal infections and highlighting the specific role of dectin-1 in human mucosal antifungal defense.
Selo DaSilva