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

Nat Immunol. 2007 Jan;8(1):31-8. doi: 10.1038/ni1408. Epub 2006 Dec 10.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Candida / immunology*
  • Candidiasis / immunology*
  • Candidiasis / prevention & control
  • Female
  • Genetic Predisposition to Disease
  • Lectins, C-Type
  • Leukocytes / immunology
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Membrane Proteins / physiology*
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Nerve Tissue Proteins / physiology*
  • beta-Glucans / immunology*
  • beta-Glucans / metabolism


  • Lectins, C-Type
  • Membrane Proteins
  • Nerve Tissue Proteins
  • beta-Glucans
  • dectin 1