伯氏疟原虫感染小鼠脑型疟疾的遗传分析。

Sabrina Torre, David Langlais, Philippe Gros
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引用次数: 11

摘要

疟疾是一种常见的,有时是致命的疾病,由疟原虫感染引起。脑型疟疾是恶性疟原虫感染最严重的并发症,其特点是复杂的免疫病理,包括显著的神经炎症。实验小鼠感染伯氏疟原虫(Plasmodium berghei ANKA)致脑性疟疾(ECM)模型已被大量用于研究单个基因、蛋白和通路在CM发病机制中的作用,包括可能的神经炎症作用。在这篇综述中,我们讨论了伯氏疟原虫ANKA感染模型来研究人类CM,并总结了在该模型中评估的所有宿主遗传效应(定位位点,单基因)在CM发病中的作用。综上所述,这些研究记录了ECM病理炎症所需的免疫系统的许多方面,但也确定了CM和以神经炎症为特征的疾病的潜在治疗干预的新途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.

Malaria is a common and sometimes fatal disease caused by infection with Plasmodium parasites. Cerebral malaria (CM) is a most severe complication of infection with Plasmodium falciparum parasites which features a complex immunopathology that includes a prominent neuroinflammation. The experimental mouse model of cerebral malaria (ECM) induced by infection with Plasmodium berghei ANKA has been used abundantly to study the role of single genes, proteins and pathways in the pathogenesis of CM, including a possible contribution to neuroinflammation. In this review, we discuss the Plasmodium berghei ANKA infection model to study human CM, and we provide a summary of all host genetic effects (mapped loci, single genes) whose role in CM pathogenesis has been assessed in this model. Taken together, the reviewed studies document the many aspects of the immune system that are required for pathological inflammation in ECM, but also identify novel avenues for potential therapeutic intervention in CM and in diseases which feature neuroinflammation.

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