Candida and host determinants of susceptibility to invasive candidiasis

Studies in mice revealed that IFN-γ and IL-17α produced by Th1 and Th17 lymphocytes were essential for vaccine-induced protection, via Ccl3- and Cxcl1-mediated neutrophil recruitment to sites of infection, which resulted in decreased Candida tissue burden [8]. [...]a fundamental C. albicans virulence factor is its ability to transition between unicellular yeast cells and filamentous growth during infection; in fact, it is the interchange between these morphotypes that is critical for pathogenesis, as strains locked either in the yeast or the filamentous forms have attenuated virulence in vivo [9], [10]. [...]complement deficiencies and MyD88 mutations do not appear to confer a significant risk for invasive candidiasis in humans as opposed to mice [26]; however, a recent large cohort study demonstrated that TLR1 single nucleotide polymorphisms in Caucasian patients were associated with heightened risk for development of invasive candidiasis, suggesting that TLR signaling may contribute to optimal anti-Candida immunity in humans [29].