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• W2081454436 abstract "Abstract The functional consequences of treating human monocytes with purified and chemically characterized Candida albicans β-glucan—a major microbial pathogen associated molecular pattern—on their differentiation into dendritic cells (DC) were investigated. We show here that β-glucan-treated monocytes differentiated into mature DC (Glu-MoDC) with altered phenotype and functional behavior, similarly to DC derived from C. albicans germ-tubes-infected monocytes (Gt-MoDC). They failed to express CD1a and to up-regulate CD80 and DR molecules. Moreover, they produced IL-10 but not IL-12 and primed naive T cells without inducing their functional polarization into effector cells. Since C. albicans β-glucan is a mixture of both β-(1,3) and β-(1,6) glucan, we investigated their relative contribution by the use of non-Candida β-glucan structural analogs. We found that high molecular weight (MW) glucans β−(1,6) pustulan and β-(1,3) curdlan totally mimicked the effect of C. albicans β-glucan, while the low MW β-(1,3) glucan laminarin did not have any effect. Because β-glucan is a common constituent of all fungi and is abundantly released in vivo during systemic fungal infection, this novel effect of β-glucan has potential implications for host-parasite relationship in candidiasis and other mycoses. In particular, our data suggest that β-glucan could bias noninfected, bystander monocytes, thus aggravating the general immunodeficiency, predisposing to systemic fungal infection." @default.
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• W2081454436 date "2007-07-26" @default.
• W2081454436 modified "2023-10-01" @default.
• W2081454436 title "β-Glucan of<i>Candida albicans</i>cell wall causes the subversion of human monocyte differentiation into dendritic cells" @default.
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• W2081454436 doi "https://doi.org/10.1189/jlb.0307160" @default.
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