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变异型克雅氏病发病机制中感染性朊蛋白的肠道进入机制

Mechanism of intestinal entry of infectious prion protein in the pathogenesis of variant Creutzfeldt-Jakob disease.

作者信息

Ghosh Subrata

机构信息

Department of Gastroenterology, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, UK.

出版信息

Adv Drug Deliv Rev. 2004 Apr 19;56(6):915-20. doi: 10.1016/j.addr.2003.10.035.

DOI:10.1016/j.addr.2003.10.035
PMID:15063598
Abstract

The pathogenesis of variant Creutzfeldt-Jakob disease (vCJD) is most likely to be dependent on intestinal entry of orally ingested infectious prion proteins, though tonsils or other oral portals of entry are possible. The exact route of entry of infectious prion proteins is uncertain but receptors for prion proteins such as laminin receptor precursor (LRP) may be expressed on intestinal brush border. Cellular prion protein (PrP(c)) is expressed on intestinal enteric nervous system and is separated by a single layer of epithelial cells from ingested infectious prion proteins. Intestinal M cells in the Peyer's patches may also transcytose prion proteins which may be transported to the lymphatic system by migrating dendritic cells underlying the M cells. The relative importance of the several potential portals of intestinal entry of infectious prion proteins is uncertain but may determine susceptibility of the population and also potential preventive strategies.

摘要

变异型克雅氏病(vCJD)的发病机制很可能依赖于经口摄入的传染性朊病毒蛋白通过肠道进入体内,不过扁桃体或其他口腔进入途径也有可能。传染性朊病毒蛋白的确切进入途径尚不确定,但诸如层粘连蛋白受体前体(LRP)等朊病毒蛋白的受体可能在肠道刷状缘表达。细胞朊病毒蛋白(PrP(c))在肠道肠神经系统表达,与摄入的传染性朊病毒蛋白被单层上皮细胞分隔开。派尔集合淋巴结中的肠道M细胞也可能转胞吞朊病毒蛋白,这些蛋白可能通过M细胞下方迁移的树突状细胞被转运至淋巴系统。传染性朊病毒蛋白几种潜在肠道进入途径的相对重要性尚不确定,但可能决定人群的易感性以及潜在的预防策略。

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