Immune Sensing of Candida Albicans Requires Cooperative Recognition of Mannans and Glucans by Lectin and Toll-Like Receptors

Creator(s)

Mihai Netea, Radboud University Nijmegen Medical Centre
Neil A.R. Gow, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Carol A. Munro, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Steven Bates, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Claire Collins, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Gerben Ferwerda, Radboud University Nijmegen Medical Centre
Richard P. Hobson, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Gwyneth Bertram, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
H. Bleddyn Hughes, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Trees Jansen, Radboud University Nijmegen Medical Centre
Liesbeth Jacobs, Radboud University Nijmegen Medical Centre
Ed T. Buurman, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Karlijn Gijzen, Radboud University Nijmegen Medical Centre
David L. Williams, East Tennessee State UniversityFollow
Ruurd Torensma, Radboud University Nijmegen Medical Centre
Alistair McKinnon, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Donna M. MacCallum, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Frank C. Odds, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Jos W.M. Van Der Meer, Radboud University Nijmegen Medical Centre
Alistair J.P. Brown, University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Bart Jan Kullberg, Radboud University Nijmegen Medical Centre

Document Type

Article

Publication Date

6-1-2006

Description

The fungal pathogen Candida albicans has a multilayered cell wall composed of an outer layer of proteins glycosylated with N- or O-linked mannosyl residues and an inner skeletal layer of β-glucans and chitin. We demonstrate that cytokine production by human mononuclear cells or murine macrophages was markedly reduced when stimulated by C. albicans mutants defective in mannosylation. Recognition of mannosyl residues was mediated by mannose receptor binding to N-linked mannosyl residues and by TLR4 binding to O-linked mannosyl residues. Residual cytokine production was mediated by recognition of β-glucan by the dectin-1/TLR2 receptor complex. C. albicans mutants with a cell wall defective in mannosyl residues were less virulent in experimental disseminated candidiasis and elicited reduced cytokine production in vivo. We concluded that recognition of C. albicans by monocytes/macrophages is mediated by 3 recognition systems of differing importance, each of which senses specific layers of the C. albicans cell wall.

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