克氏锥虫致宿主细胞侵袭的分子机制。
Molecular mechanisms of host cell invasion by Trypanosoma cruzi.
机构信息
Department of Pediatrics, Northwestern University, Chicago, IL 60611, USA.
出版信息
Exp Parasitol. 2010 Nov;126(3):283-91. doi: 10.1016/j.exppara.2010.06.023. Epub 2010 Jun 18.
Abstract
The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.
摘要
原生动物寄生虫克氏锥虫，恰加斯病的病原体，是一种必需的细胞内原生动物病原体。重叠的机制确保了成功的感染，但这些细胞事件与临床疾病之间的关系仍然不清楚。这篇综述从细胞表面相互作用、细胞内信号转导、宿主细胞骨架和内体区室的调节以及感染的细胞内先天免疫反应的角度探讨了细胞入侵的过程。
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Identification of glycoproteins targeted by Trypanosoma cruzi trans-sialidase, a virulence factor that disturbs lymphocyte glycosylation.鉴定克氏锥虫转涎糖基酶（一种扰乱淋巴细胞糖基化的毒力因子）的糖蛋白靶标。
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The innate immune response to Trypanosoma cruzi infection.对克氏锥虫感染的固有免疫反应。
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