Dectin-1 escape by fungal dimorphism

Sigrid E.M. Heinsbroek, Gordon D. Brown, Siamon Gordon*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

42 Scopus citations

Abstract

Candida albicans, a medically important fungus, exists primarily as yeast and filamentous forms. Its cell wall is rich in β-glucans, which are recognized by a lectin-like innate immune receptor, Dectin-1. A recent study shows that exposure of glucan, by yeasts but not filaments, determines Dectin-1-dependent uptake by macrophages, and thus represents a novel immune evasion mechanism. Here, we discuss the insights these results provide in relation to macrophage interactions with C. albicans and pathogen entry.

Original languageEnglish
Pages (from-to)352-354
Number of pages3
JournalTrends in Immunology
Volume26
Issue number7
DOIs
StatePublished - 07 2005
Externally publishedYes

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