The role of the cytoskeleton in host cell invasion by Toxoplasma gondii.

Behring Institute Mitteilungen Pub Date : 1997-03-01
J Dobrowolski, L D Sibley
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Abstract

The protozoan parasite Toxoplasma gondii provides a model system for studying invasion by intracellular parasites belonging to the phylum Apicomplexa. Taking advantage of the versatility of T. gondii for genetic and cell biological studies, we have shown that parasite motility and cell invasion are powered by an actin-myosin based motor in the parasite. Unlike bacterial cell uptake, parasite invasion does not involve significant alterations in the host cell cytoskeleton. Instead, invasion is an active process of penetration into the host cell by the parasite. The force for cell penetration is provided by a unique form of substrate-dependent motility termed gliding. Gliding motility is characterized by the rearward capping of surface membrane proteins that propels the parasite forward in a helical spiral. Both actin and myosin are localized beneath the plasma membrane in the parasite where they presumably combine to produce the force necessary for motility. During cell invasion, the rearward capping of cell surface receptors envelopes the parasite in a unique vacuole derived from the host cell plasma membrane. This system offers insights into force generation and motility in a simple organism that is also an important human pathogen.

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细胞骨架在刚地弓形虫侵袭宿主细胞中的作用。
原生动物弓形虫为研究顶复门细胞内寄生虫的入侵提供了一个模型系统。利用弓形虫的多功能性进行遗传和细胞生物学研究,我们已经证明寄生虫的运动和细胞入侵是由寄生虫中基于肌动蛋白-肌球蛋白的运动驱动的。与细菌细胞摄取不同,寄生虫入侵不涉及宿主细胞骨架的重大改变。相反,入侵是寄生虫侵入宿主细胞的一个主动过程。细胞穿透的力是由一种独特的依赖于基质的运动形式提供的,称为滑动。滑翔运动的特点是表面膜蛋白的后盖推动寄生虫以螺旋形向前。肌动蛋白和肌凝蛋白都位于寄生虫的质膜下,它们可能在那里结合产生运动所需的力量。在细胞入侵过程中,细胞表面受体的后盖将寄生虫包裹在一个来自宿主细胞质膜的独特液泡中。该系统提供了对力的产生和运动的见解,在一个简单的有机体,也是一个重要的人类病原体。
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The role of chemokines and accessory cells in the immunoregulation of cutaneous leishmaniasis. Schistosoma mansoni infection induces a type 1 CD8+ cell response. Malaria sporozoites and chylomicron remnants compete for binding sites in the liver. The role of the cytoskeleton in host cell invasion by Toxoplasma gondii. Reactivation of chronic toxoplasmosis: is there a link to strain-specific differences in the parasite?
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