Article abstract
Nature Immunology 8, 31 - 38 (2006)
Published online: 10 December 2006 | doi:10.1038/ni1408
Dectin-1 is required for 
-glucan recognition and control of fungal infection
Philip R Taylor1,5, S Vicky Tsoni2,5, Janet A Willment2, Kevin M Dennehy2, Marcela Rosas1, Helen Findon3, Ken Haynes3, Chad Steele4, Marina Botto3, Siamon Gordon1 & Gordon D Brown2
Abstract
-Glucan is one of the most abundant polysaccharides in fungal pathogens, yet its importance in antifungal immunity is unclear. Here we show that deficiency of dectin-1, the myeloid receptor for -glucan, rendered mice susceptible to infection with Candida albicans. Dectin-1-deficient leukocytes demonstrated significantly impaired responses to fungi even in the presence of opsonins. Impaired leukocyte responses were manifested in vivo by reduced inflammatory cell recruitment after fungal infection, resulting in substantially increased fungal burdens and enhanced fungal dissemination. Our results establish a fundamental function for -glucan recognition by dectin-1 in antifungal immunity and demonstrate a signaling non–Toll-like pattern-recognition receptor required for the induction of protective immune responses.
- Sir William Dunn School of Pathology, University of Oxford, Oxford OX13RE, UK.
- Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town 7925, South Africa.
- Imperial College School of Medicine, Hammersmith Campus, London W12 0NN, UK.
- Department of Pediatrics, Division of Pulmonology, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
- These authors contributed equally to this work.
Correspondence to: Gordon D Brown2 e-mail: gordon.brown@mweb.co.za
