Figure 1.

Mucosal innate immunity to Candida albicans. Recognition of C. albicans by epithelial cells is mainly mediated by the β-glucan receptor Eph2A. This leads to the activation of epithelial cells that greatly depends on fungal morphology and secretion of the hyphal toxin candidalysin. While yeast cells activate PI3K/Akt and NF-κB, with a weaker activation of p38, JNK, and ERK1/2 MAPK signaling pathways, hyphal growth and the release of candidalysin to the infection pocket promote a sustained, strong activation of all three MAPK pathways. The first leads to the recruitment of c-Jun, with as-yet unknown transcriptional consequences. Hyphal activation, however, induces c-Fos activation, leading to the release of pro-inflammatory molecules and antimicrobial peptides. These molecules will eventually help to clear fungal invasion and recruit more immune cells to the infection foci, such as neutrophils, macrophages and innate Th17 cells.