Dectin-1 escape by fungal dimorphism

Candida albicans, a medically important fungus, exists primarily as yeast and filamentous forms. Its cell wall is rich in β-glucans, which are recognized by a lectin-like innate immune receptor, Dectin-1. A recent study shows that exposure of glucan, by yeasts but not filaments, determines Dectin-1-dependent uptake by macrophages, and thus represents a novel immune evasion mechanism. Here, we discuss the insights these results provide in relation to macrophage interactions with C. albicans and pathogen entry.