Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 W. Carson St., Torrance, CA 90502, USA.
Cytokine. 2012 Apr;58(1):129-32. doi: 10.1016/j.cyto.2011.09.018. Epub 2011 Oct 19.
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.
念珠菌属是人类最常见的黏膜和播散性真菌感染的病原体。利用突变株小鼠进行的研究为宿主防御念珠菌病中树突状细胞识别受体 1（dectin-1）、CARD9 和 Th17 细胞因子的作用提供了初步信息。最近的技术进步已经确定了导致人类易患念珠菌感染的特定基因突变。对这些突变个体的分析表明，dectin-1 对宿主防御外阴阴道念珠菌病和胃肠道念珠菌定植至关重要。这些研究还表明 CARD9 对预防黏膜和播散性念珠菌病很重要，而 Th17 反应对防御黏膜皮肤念珠菌病是必需的。本文综述了人类遗传缺陷导致念珠菌易感性增加的最新研究，并讨论了这些研究如何为宿主防御不同类型的念珠菌感染提供新的见解。
