Dectin-1 mediates macrophage recognition of Candida albicans yeast but not filaments. EMBO J 2005 Mar 23;24(6):1277-86
Date
02/25/2005Pubmed ID
15729357Pubmed Central ID
PMC556398DOI
10.1038/sj.emboj.7600594Scopus ID
2-s2.0-17144370549 (requires institutional sign-in at Scopus site) 576 CitationsAbstract
The ability of Candida albicans to rapidly and reversibly switch between yeast and filamentous morphologies is crucial to pathogenicity, and it is thought that the filamentous morphology provides some advantage during interaction with the mammalian immune system. Dectin-1 is a receptor that binds beta-glucans and is important for macrophage phagocytosis of fungi. The receptor also collaborates with Toll-like receptors for inflammatory activation of phagocytes by fungi. We show that yeast cell wall beta-glucan is largely shielded from Dectin-1 by outer wall components. However, the normal mechanisms of yeast budding and cell separation create permanent scars which expose sufficient beta-glucan to trigger antimicrobial responses through Dectin-1, including phagocytosis and activation of reactive oxygen production. During filamentous growth, no cell separation or subsequent beta-glucan exposure occurs, and the pathogen fails to activate Dectin-1. The data demonstrate a mechanism by which C. albicans shape alone directly contributes to the method by which phagocytes recognize the fungus.
Author List
Gantner BN, Simmons RM, Underhill DMAuthor
Benjamin N. Gantner PhD Assistant Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCandida albicans
Cell Line
Glucans
Hyphae
Lectins, C-Type
Macrophage Activation
Macrophages
Membrane Proteins
Mice
Nerve Tissue Proteins
Phagocytosis
Polysaccharides
Reactive Oxygen Species
Zymosan
beta-Glucans
