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疟疾糖基磷脂酰肌醇(GPI)介导的Toll样受体(TLR)细胞信号传导

TLR-mediated cell signaling by malaria GPIs.

作者信息

Gowda D Channe

机构信息

Department of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.

出版信息

Trends Parasitol. 2007 Dec;23(12):596-604. doi: 10.1016/j.pt.2007.09.003. Epub 2007 Nov 5.

Abstract

Proinflammatory responses to malaria have crucial roles in controlling parasite growth and disease pathogenesis. The glycosylphosphatidylinositol (GPI) of Plasmodium falciparum is thought to be an important factor in the induction of proinflammatory responses. The GPI induces host cellular responses mainly through Toll-like receptor (TLR)2/MyD88-mediated signaling. Knowledge of the parasite-host factors involved in activating and regulating innate immune responses and of the associated signaling mechanisms is likely to provide insights into the modulation of parasite-specific adaptive immunity and offer targets for the development of novel therapeutics or a vaccine for malaria. This article focuses on the malaria GPI-mediated cell-signaling mechanisms.

摘要

对疟疾的促炎反应在控制寄生虫生长和疾病发病机制中起着关键作用。恶性疟原虫的糖基磷脂酰肌醇(GPI)被认为是诱导促炎反应的一个重要因素。GPI主要通过Toll样受体(TLR)2/髓样分化因子88(MyD88)介导的信号传导诱导宿主细胞反应。了解参与激活和调节先天免疫反应的寄生虫-宿主因子以及相关的信号传导机制,可能会为调节寄生虫特异性适应性免疫提供见解,并为开发新型疟疾治疗药物或疫苗提供靶点。本文重点关注疟疾GPI介导的细胞信号传导机制。

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