Dectin-1 mediates the biological effects of beta-glucans

Gordon D Brown, Jurgen Herre, David L Williams, Janet A Willment, Andrew S J Marshall, Siamon Gordon

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852 Citations (Scopus)

Abstract

The ability of fungal-derived beta-glucan particles to induce leukocyte activation and the production of inflammatory mediators, such as tumor necrosis factor (TNF)-alpha, is a well characterized phenomenon. Although efforts have been made to understand how these carbohydrate polymers exert their immunomodulatory effects, the receptors involved in generating these responses are unknown. Here we show that Dectin-1 mediates the production of TNF-alpha in response to zymosan and live fungal pathogens, an activity that occurs at the cell surface and requires the cytoplasmic tail and immunoreceptor tyrosine activation motif of Dectin-1 as well as Toll-like receptor (TLR)-2 and Myd88. This is the first demonstration that the inflammatory response to pathogens requires recognition by a specific receptor in addition to the TLRs. Furthermore, these studies implicate Dectin-1 in the production of TNF-alpha in response to fungi, a critical step required for the successful control of these pathogens.
Original languageEnglish
Pages (from-to)1119-1124
Number of pages6
JournalJournal of Experimental Medicine
Volume197
Issue number9
Early online date28 Apr 2003
DOIs
Publication statusPublished - 5 May 2003

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Keywords

  • Animals
  • Candida albicans
  • Glucans
  • Macrophages
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Nerve Tissue Proteins
  • Tumor Necrosis Factor-alpha
  • Zymosan

Cite this

Brown, G. D., Herre, J., Williams, D. L., Willment, J. A., Marshall, A. S. J., & Gordon, S. (2003). Dectin-1 mediates the biological effects of beta-glucans. Journal of Experimental Medicine, 197(9), 1119-1124. https://doi.org/10.1084/jem.20021890