title: Dectin-1 escape by fungal dimorphism.
abstract: Candida albicans, a medically important fungus, exists primarily as yeast and filamentous forms. Its cell wall is rich in beta-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.
authors.affiliation: Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, UK OX1 3RE.
authors.forename: Sigrid E M
authors.initials: SE
authors.lastname: Heinsbroek
authors.forename: Gordon D
authors.initials: GD
authors.lastname: Brown
authors.forename: Siamon
authors.initials: S
authors.lastname: Gordon
mesh_terms: D000818:Animals; D002176:Candida albicans / Q000254:growth & development / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D007113:Immunity, Innate; D037181:Lectins, C-Type; D017737:Macrophages, Peritoneal / Q000276:immunology / Q000382:microbiology; D008565:Membrane Proteins / Q000276:immunology*; D009419:Nerve Tissue Proteins / Q000276:immunology*; D010587:Phagocytosis; D014774:Virulence; D000099181:Dectin-1
chemical_list: D037181:Lectins, C-Type; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D000099181:Dectin-1