The analysis of individuals with these mutations demonstrates that dectin-1 is critical for the host defense against vulvovaginal candidiasis and candidal colonization of the gastrointestinal tract.
This study suggests that PD exerts inhibitory effects on C. albicans proliferation, adhesion and inflammation and simultaneously downregulates the expression levels of important genes and proteins associated with the Dectin-1 pathway, highlighting the potential application of PD to improve the clinical management of VVC.
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.