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Dectin-1 is a major beta-glucan receptor on macrophages

Brown, Gordon D., Taylor, Philip Russel ORCID: https://orcid.org/0000-0003-0163-1421, Reid, Delyth M., Willment, Janet A., Williams, David L., Martinez-Pomares, Luisa, Wong, Simon Y. C. and Gordon, Siamon 2002. Dectin-1 is a major beta-glucan receptor on macrophages. Journal of Experimental Medicine 196 (3) , pp. 407-12. 10.1084/jem.20020470

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Abstract

Zymosan is a ?-glucan– and mannan-rich particle that is widely used as a cellular activator for examining the numerous responses effected by phagocytes. The macrophage mannose receptor (MR) and complement receptor 3 (CR3) have historically been considered the major macrophage lectins involved in the nonopsonic recognition of these yeast-derived particles. Using specific carbohydrate inhibitors, we show that a ?-glucan receptor, but not the MR, is a predominant receptor involved in this process. Furthermore, nonopsonic zymosan binding was unaffected by genetic CD11b deficiency or a blocking monoclonal antibody (mAb) against CR3, demonstrating that CR3 was not the ?-glucan receptor mediating this activity. To address the role of the recently described ?-glucan receptor, Dectin-1, we generated a novel anti–Dectin-1 mAb, 2A11. Using this mAb, we show here that Dectin-1 was almost exclusively responsible for the ?-glucan–dependent, nonopsonic recognition of zymosan by primary macro-phages. These findings define Dectin-1 as the leukocyte ?-glucan receptor, first described over 50 years ago, and resolves the long-standing controversy regarding the identity of this important molecule. Furthermore, these results identify Dectin-1 as a new target for examining the immunomodulatory properties of ?-glucans for therapeutic drug design.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: Q Science > QR Microbiology
R Medicine > R Medicine (General)
R Medicine > RB Pathology
Additional Information: Publisher’s copyright requirements: “Ownership of copyright in the Work remains with the authors. The Authors retain the non-exclusive right to do anything they want with the Work, so long as the Authors provide attribution to the place of original publication. The retained right specifically includes the right to post the Work on the authors’ or their institutions’ web sites.” See: http://www.rupress.org/site/subscriptions/terms.xhtml
Publisher: Rockefeller University Press
ISSN: 1540-9538
Last Modified: 04 May 2023 15:36
URI: https://orca.cardiff.ac.uk/id/eprint/203

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