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首页> 外文期刊>The Journal of Infectious Diseases >Role of Mannose-Binding Lectin in the Innate Defense against Candida albicans: Enhancement of Complement Activation, but Lack of Opsonic Function, in Phagocytosis by Human Dendritic Cells.
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Role of Mannose-Binding Lectin in the Innate Defense against Candida albicans: Enhancement of Complement Activation, but Lack of Opsonic Function, in Phagocytosis by Human Dendritic Cells.

机译:甘露糖结合凝集素在抵抗白色念珠菌的先天防御中的作用:在人类树突状细胞吞噬作用中补体激活的增强,但缺乏调理功能。

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摘要

Mannose-binding lectin (MBL) is a serum collectin believed to be of importance in innate immunity. We have investigated the role of MBL in the first-line defense against Candida albicans, an opportunistic fungal pathogen. MBL bound C. albicans via its lectin domain, resulting in agglutination of the organisms upon their outgrowth of hyphae. In a human in vitro MBL system, deposition of C4 fragments on C. albicans was increased when exogenous MBL was added to serum samples from MBL-deficient individuals. Similar enhancement of deposition of iC3b also was observed. MBL and enhanced opsonic C3 fragments mediated by MBL did not facilitate opsonophagocytosis of the organisms by monocyte-derived dendritic cells (DCs). However, MBL was found to inhibit the growth of C. albicans independently of complement activation, although, with complement activation, further inhibition was observed. We concluded that MBL plays an important role in the first-line defense against C. albicans without the need for opsonophagocytosis by DCs, in which a direct interaction of MBL with C. albicans results in agglutination and accelerated complement activation via the lectin pathway, leading to inhibition of growth.
机译:甘露糖结合凝集素(MBL)是一种血清收集素,据信在先天免疫中很重要。我们调查了MBL在针对白色念珠菌(一种机会性真菌病原体)的一线防御中的作用。 MBL通过其凝集素结构域与白色念珠菌结合,导致微生物在菌丝生长后发生凝集。在人体外MBL系统中,将外源MBL添加到MBL缺陷个体的血清样本中时,C4片段在白色念珠菌上的沉积增加。还观察到iC3b沉积的类似增强。 MBL介导的MBL和增强的调理性C3片段不能促进单核细胞衍生的树突状细胞(DC)对生物体的调理吞噬作用。然而,发现MBL独立于补体激活抑制白念珠菌的生长,尽管通过补体激活观察到了进一步的抑制。我们得出的结论是,MBL在针对白色念珠菌的一线防御中起着重要作用,而无需DC进行调理吞噬作用,其中MBL与白色念珠菌的直接相互作用导致凝集和通过凝集素途径加速补体激活,从而导致抑制生长。

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