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真菌聚糖如何通过Toll样受体调节血小板活化,从而有助于逃避免疫反应。

How Fungal Glycans Modulate Platelet Activation via Toll-Like Receptors Contributing to the Escape of from the Immune Response.

作者信息

Jawhara Samir

机构信息

Institut National de la Santé et de la Recherche Médicale U1285, Faculté de Médecine, 1 Place Verdun, 59000 Lille, France.

UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, Centre National de la Recherche Scientifique, University of Lille, 59000 Lille, France.

出版信息

Antibiotics (Basel). 2020 Jul 7;9(7):385. doi: 10.3390/antibiotics9070385.

Abstract

Platelets are essential for vascular repair and for the maintenance of blood homeostasis. They contribute to the immune defence of the host against many infections caused by bacteria, viruses and fungi. Following infection, platelet function is modified, and these cells form aggregates with microorganisms leading, to a decrease in the level of circulating platelets. During candidaemia, mannans, β-glucans and chitin, exposed on the cell wall of , an opportunistic pathogenic yeast of humans, play an important role in modulation of the host response. These fungal polysaccharides are released into the circulation during infection and their detection allows the early diagnosis of invasive fungal infections. However, their role in the modulation of the immune response and, in particular, that of platelets, is not well understood. The structure and solubility of glycans play an important role in the orientation of the immune response of the host. This short review focuses on the effect of fungal β-glucans and chitin on platelet activation and how these glycans modulate platelet activity via Toll-like receptors, contributing to the escape of from the immune response.

摘要

血小板对于血管修复和维持血液稳态至关重要。它们有助于宿主对细菌、病毒和真菌引起的许多感染进行免疫防御。感染后,血小板功能会发生改变,这些细胞会与微生物形成聚集体,导致循环血小板水平下降。在念珠菌血症期间,人类机会致病性酵母细胞壁上暴露的甘露聚糖、β-葡聚糖和几丁质在调节宿主反应中起重要作用。这些真菌多糖在感染期间释放到循环中,对它们的检测有助于侵袭性真菌感染的早期诊断。然而,它们在调节免疫反应,特别是血小板免疫反应中的作用尚不清楚。聚糖的结构和溶解性在宿主免疫反应的导向中起重要作用。本简短综述重点关注真菌β-葡聚糖和几丁质对血小板活化的影响,以及这些聚糖如何通过Toll样受体调节血小板活性,从而导致念珠菌逃避免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7771/7399910/3f201da2cee6/antibiotics-09-00385-g001.jpg

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