原生动物寄生虫利什曼原虫对宿主细胞信号传导的破坏。

Subversion of host cell signalling by the protozoan parasite Leishmania.

作者信息

Gregory D J, Olivier M

机构信息

Centre for the Study of Host Resistance, Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.

出版信息

Parasitology. 2005;130 Suppl:S27-35. doi: 10.1017/S0031182005008139.

Abstract

The protozoa Leishmania spp. are obligate intracellular parasites that inhabit the macrophages of their host. Since macrophages are specialized for the identification and destruction of invading pathogens, both directly and by triggering an innate immune response, Leishmania have evolved a number of mechanisms for suppressing some critical macrophage activities. In this review, we discuss how various species of Leishmania distort the host macrophage's own signalling pathways to repress the expression of various cytokines and microbicidal molecules (nitric oxide and reactive oxygen species), and antigen presentation. In particular, we describe how MAP Kinase and JAK/STAT cascades are repressed, and intracellular Ca2+ and the activities of protein tyrosine phosphatases, in particular SHP-1, are elevated.

摘要

利什曼原虫属原生动物是专性细胞内寄生虫,寄生于宿主的巨噬细胞中。由于巨噬细胞专门用于直接以及通过触发先天性免疫反应来识别和破坏入侵的病原体,利什曼原虫已经进化出多种机制来抑制巨噬细胞的一些关键活动。在本综述中,我们讨论了不同种类的利什曼原虫如何扭曲宿主巨噬细胞自身的信号通路,以抑制各种细胞因子和杀菌分子(一氧化氮和活性氧)的表达以及抗原呈递。特别是,我们描述了丝裂原活化蛋白激酶(MAP Kinase)和JAK/STAT级联反应是如何被抑制的,以及细胞内钙离子和蛋白酪氨酸磷酸酶(尤其是SHP-1)的活性是如何升高的。

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