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JC多瘤病毒(JCV)与单克隆抗体:是友还是潜在的敌?

JC polyomavirus (JCV) and monoclonal antibodies: friends or potential foes?

作者信息

Diotti Roberta Antonia, Nakanishi Akira, Clementi Nicola, Mancini Nicasio, Criscuolo Elena, Solforosi Laura, Clementi Massimo

机构信息

Microbiology and Virology Institute, Vita-Salute San Raffaele University, Via Olgettina 58, 20132 Milan, Italy.

出版信息

Clin Dev Immunol. 2013;2013:967581. doi: 10.1155/2013/967581. Epub 2013 Jun 25.

DOI:10.1155/2013/967581
PMID:23878587
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3708391/
Abstract

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system (CNS), observed in immunodeficient patients and caused by JC virus ((JCV), also called JC polyomavirus (JCPyV)). After the HIV pandemic and the introduction of immunomodulatory therapy, the PML incidence significantly increased. The correlation between the use of natalizumab, a drug used in multiple sclerosis (MS), and the PML development of particular relevance. The high incidence of PML in natalizumab-treated patients has highlighted the importance of two factors: the need of PML risk stratification among natalizumab-treated patients and the need of effective therapeutic options. In this review, we discuss these two needs under the light of the major viral models of PML etiopathogenesis.

摘要

进行性多灶性白质脑病(PML)是一种中枢神经系统(CNS)脱髓鞘疾病,见于免疫缺陷患者,由JC病毒(JCV,也称为JC多瘤病毒(JCPyV))引起。在艾滋病大流行和免疫调节治疗引入后,PML的发病率显著增加。用于治疗多发性硬化症(MS)的那他珠单抗的使用与PML发生之间的相关性尤为重要。那他珠单抗治疗患者中PML的高发病率凸显了两个因素的重要性:对那他珠单抗治疗患者进行PML风险分层的必要性以及有效治疗选择的必要性。在本综述中,我们根据PML发病机制的主要病毒模型来讨论这两个需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/2d3d0269d565/CDI2013-967581.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/53aeca06a5d9/CDI2013-967581.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/932fe24e8575/CDI2013-967581.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/2d3d0269d565/CDI2013-967581.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/53aeca06a5d9/CDI2013-967581.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/932fe24e8575/CDI2013-967581.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41c8/3708391/2d3d0269d565/CDI2013-967581.003.jpg

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Granzyme B-inhibitor serpina3n induces neuroprotection in vitro and in vivo.颗粒酶B抑制剂丝氨酸蛋白酶抑制剂3N在体外和体内均具有神经保护作用。
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Inflammatory bowel disease: an increased risk factor for neurologic complications.炎症性肠病:神经系统并发症的一个风险增加因素。
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