Candida species are major causes of infections affecting either body surfaces or the deep tissues. Candida is a complex pathogen and the immune system uses various cells, cell surface receptors and signalling pathways to trigger an efficient host defence. Host-Candida interaction can result either in rapid elimination of the pathogen or the persistence of the pathogen in immunocompromised patients, leading to either chronic mucocutanous candidiasis or invasive candidiasis. Here, we discuss the molecular basis of receptor-mediated recognition and uptake of non-opsonized Candida and we describe the relative role of these receptors in initiating inflammation. In addition, the consequence of genetic defects in dectin-1 and dectin-1-mediated signalling and the role of Th17-dependent mechanisms for the mucosal antifungal defence are discussed.
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