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

Research output: Contribution to journalArticle

833 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

Fingerprint

beta-Glucans
Tumor Necrosis Factor-alpha
Beta Particles
Toll-Like Receptor 2
Zymosan
Tyrosine
Polymers
Leukocytes
Fungi
Carbohydrates
dectin 1

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

Dectin-1 mediates the biological effects of beta-glucans. / Brown, Gordon D; Herre, Jurgen; Williams, David L; Willment, Janet A; Marshall, Andrew S J; Gordon, Siamon.

In: Journal of Experimental Medicine, Vol. 197, No. 9, 05.05.2003, p. 1119-1124.

Research output: Contribution to journalArticle

Brown, GD, Herre, J, Williams, DL, Willment, JA, Marshall, ASJ & Gordon, S 2003, 'Dectin-1 mediates the biological effects of beta-glucans', Journal of Experimental Medicine, vol. 197, no. 9, pp. 1119-1124. https://doi.org/10.1084/jem.20021890
Brown GD, Herre J, Williams DL, Willment JA, Marshall ASJ, Gordon S. Dectin-1 mediates the biological effects of beta-glucans. Journal of Experimental Medicine. 2003 May 5;197(9):1119-1124. https://doi.org/10.1084/jem.20021890
Brown, Gordon D ; Herre, Jurgen ; Williams, David L ; Willment, Janet A ; Marshall, Andrew S J ; Gordon, Siamon. / Dectin-1 mediates the biological effects of beta-glucans. In: Journal of Experimental Medicine. 2003 ; Vol. 197, No. 9. pp. 1119-1124.
@article{8c7109b70db848fbb963599ac5b0317e,
title = "Dectin-1 mediates the biological effects of beta-glucans",
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.",
keywords = "Animals, Candida albicans, Glucans, Macrophages, Membrane Proteins, Mice, Mice, Inbred C57BL, Nerve Tissue Proteins, Tumor Necrosis Factor-alpha, Zymosan",
author = "Brown, {Gordon D} and Jurgen Herre and Williams, {David L} and Willment, {Janet A} and Marshall, {Andrew S J} and Siamon Gordon",
year = "2003",
month = "5",
day = "5",
doi = "10.1084/jem.20021890",
language = "English",
volume = "197",
pages = "1119--1124",
journal = "Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "9",

}

TY - JOUR

T1 - Dectin-1 mediates the biological effects of beta-glucans

AU - Brown, Gordon D

AU - Herre, Jurgen

AU - Williams, David L

AU - Willment, Janet A

AU - Marshall, Andrew S J

AU - Gordon, Siamon

PY - 2003/5/5

Y1 - 2003/5/5

N2 - 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.

AB - 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.

KW - Animals

KW - Candida albicans

KW - Glucans

KW - Macrophages

KW - Membrane Proteins

KW - Mice

KW - Mice, Inbred C57BL

KW - Nerve Tissue Proteins

KW - Tumor Necrosis Factor-alpha

KW - Zymosan

U2 - 10.1084/jem.20021890

DO - 10.1084/jem.20021890

M3 - Article

VL - 197

SP - 1119

EP - 1124

JO - Journal of Experimental Medicine

JF - Journal of Experimental Medicine

SN - 0022-1007

IS - 9

ER -