Chronic infection by Leishmania amazonensis mediated through MAPK ERK mechanisms.
Chronic infection by Leishmania amazonensis mediated through MAPK ERK mechanisms.
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DOI：
10.1007/s12026-014-8535-y
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发表时间：
2014-08
影响因子：
4.4
通讯作者：
Petersen CA
中科院分区：
文献类型：
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作者：
Martinez PA;Petersen CA
亚马逊利什曼原虫是一种导致慢性皮肤利什曼病 (CL) 的细胞内原生动物寄生虫。 CL 是一种被忽视的热带疾病，导致全世界数百万人感染。亚马逊乳杆菌促进宿主细胞生存所必需的各种信号通路的改变。具体来说，通过寄生虫介导的细胞外信号调节激酶（ERK）磷酸化，亚马逊乳杆菌抑制细胞介导的寄生虫杀伤，并通过选择多种宿主细胞功能来促进其自身的生存。在这篇综述中，我们重点关注利什曼原虫宿主细胞信号转导改变，重点关注 1) 运动蛋白、2) 预防 NADPH 亚基磷酸化损害活性氧产生 (ROS)，以及 3) 上调 ERK 磷酸化的局部内体信号转导。本综述将重点关注利什曼原虫如何传播的机制和可能的解释。逃避宿主免疫反应采用的各个防御层。
Leishmania amazonensis is an intracellular protozoan parasite responsible for chronic cutaneous leishmaniasis (CL). CL is a neglected tropical disease responsible for infecting millions of people worldwide. L. amazonensis promotes alteration of various signaling pathways that are essential for host cell survival. Specifically, through parasite-mediated phosphorylation of extracellular signal regulated kinase (ERK), L. amazonensis inhibits cell-mediated parasite killing and promotes its own survival by co-opting multiple host cell functions. In this review we highlight Leishmania-host cell signaling alterations focusing on those specific to 1) motor proteins, 2) prevention of NADPH subunit phosphorylation impairing reactive oxygen species production (ROS), and 3) localized endosomal signaling to up-regulate ERK phosphorylation. This review will focus upon mechanisms and possible explanations as to how Leishmania spp. evades the various layers of defense employed by the host immune response.