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The Macrophage-Inducible C-Type Lectin, Mincle, Is an Essential Component of the Innate Immune Response to Candida albicans¹

Christine A. Wells^*, Judith A. Salvage-Jones^*, Xin Li, Kelly Hitchens^*, Suzanne Butcher^*, Rachael Z. Murray, Anthony G. Beckhouse^*, Yu-Lan-Sandra Lo^*, Silvia Manzanero^*, Christian Cobbold^*, Kate Schroder, Bo Ma, Sally Orr, Lauren Stewart, Daniel Lebus, Peter Sobieszczuk, David A. Hume, Jennifer Stow, Helen Blanchard^¶ and Robert B. Ashman^2,

^* National Centre for Adult Stem Cell Research, Eskitis Institute for Cell and Molecular Therapies, Griffith University, Brisbane, Queensland, Australia; School of Dentistry, University of Queensland, Brisbane, Queensland, Australia; Institute for Molecular Biosciences, University of Queensland, Brisbane, Queensland, Australia; Consortium for Functional Glycomics, Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037; and ^¶ Institute for Glycomics, Griffith University, Southport, Queensland, Australia

The recognition of carbohydrate moieties by cells of the innate immune system is emerging as an essential element in antifungal immunity, but despite the number and diversity of lectins expressed by innate immune cells, few carbohydrate receptors have been characterized. Mincle, a C-type lectin, is expressed predominantly on macrophages, and is here shown to play a role in macrophage responses to the yeast Candida albicans. After exposure to the yeast in vitro, Mincle localized to the phagocytic cup, but it was not essential for phagocytosis. In the absence of Mincle, production of TNF- by macrophages was reduced, both in vivo and in vitro. In addition, mice lacking Mincle showed a significantly increased susceptibility to systemic candidiasis. Thus, Mincle plays a novel and nonredundant role in the induction of inflammatory signaling in response to C. albicans infection.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Project Grant 455947 from the National Health and Medical Research Council of Australia, and by grants from the Australian Dental Research Foundation. Resources and collaborative efforts provided by the Consortium for Functional Glycomics were funded by National Institute of General Medical Sciences GM62116.

² Address correspondence and reprint requests to Dr. Robert B. Ashman, Oral Biology and Pathology, University of Queensland, Brisbane, Queensland, Australia 4072. E-mail address: r.ashman{at}uq.edu.au

³ Abbreviations used in this paper: PRR, pattern recognition receptor; Dectin, dendritic cell-associated lectin; Mcl, macrophage C-type lectin; ES, embryonic stem; WT, wild type; KO, knockout; Ct, cycle threshold; BMM, bone marrow-derived macrophage.

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