Dectin-1 is required for beta-glucan recognition and control of fungal infection

Philip R Taylor, S Vicky Tsoni, Janet A Willment, Kevin M Dennehy, Marcela Rosas, Helen Findon, Ken Haynes, Chad Steele, Marina Botto, Siamon Gordon, Gordon D Brown

Research output: Contribution to journalArticlepeer-review

881 Citations (Scopus)


Beta-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 beta-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 beta-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.
Original languageEnglish
Pages (from-to)31-38
Number of pages8
JournalNature Immunology
Issue number1
Early online date10 Dec 2006
Publication statusPublished - Jan 2007


  • Animals
  • Candida
  • Candidiasis
  • Female
  • Genetic Predisposition to Disease
  • Leukocytes
  • Membrane Proteins
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins
  • beta-Glucans


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