Insights from human studies into the host defense against candidiasis.
Candida spp. are the most common cause of mucosal and disseminated fungal infections in humans. Studies using mutant strains of mice have provided initial information about the roles of dectin-1, CARD9, and Th17 cytokines in the host defense against candidiasis. Recent technological advances have resulted in the identification of mutations in specific genes that predispose humans to develop candidal infection. 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. They also indicate that CARD9 is important for preventing both mucosal and disseminated candidiasis, whereas the Th17 response is necessary for the defense against mucocutaneous candidiasis. This article reviews the recent studies of genetic defects in humans that result in an increased susceptibility to candidiasis and discusses how these studies provide new insight into the host defense against different types of candidal infections.
Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 W. Carson St., Torrance, CA 90502, USA. sfiller@ucla.edu
Scott G
SG
Filler
D000818:Animals; D053468:CARD Signaling Adaptor Proteins / Q000502:physiology; D002177:Candidiasis / Q000276:immunology / Q000517:prevention & control*; D002178:Candidiasis, Chronic Mucocutaneous / Q000276:immunology / Q000517:prevention & control; D002181:Candidiasis, Vulvovaginal / Q000276:immunology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D037181:Lectins, C-Type / Q000502:physiology; D051379:Mice; D058504:Th17 Cells / Q000276:immunology; D000099181:Dectin-1
D053468:CARD Signaling Adaptor Proteins; D037181:Lectins, C-Type; D000099181:Dectin-1; C505855:CARD9 protein, human