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杜氏利什曼原虫对宿主防御的逃避:信号通路的颠覆

Evasion of Host Defence by Leishmania donovani: Subversion of Signaling Pathways.

作者信息

Shadab Md, Ali Nahid

机构信息

Infectious Diseases and Immunology Division, Indian Institute of Chemical Biology, 4, Raja S.C. Mullick Road, Kolkata 700032, India.

出版信息

Mol Biol Int. 2011;2011:343961. doi: 10.4061/2011/343961. Epub 2011 Apr 27.

DOI:10.4061/2011/343961
PMID:22091401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3199940/
Abstract

Protozoan parasites of the genus Leishmania are responsible for causing a variety of human diseases known as leishmaniasis, which range from self-healing skin lesions to severe infection of visceral organs that are often fatal if left untreated. Leishmania donovani (L. donovani), the causative agent of visceral leishmaniasis, exemplifys a devious organism that has developed the ability to invade and replicate within host macrophage. In fact, the parasite has evolved strategies to interfere with a broad range of signaling processes in macrophage that includes Protein Kinase C, the JAK2/STAT1 cascade, and the MAP Kinase pathway. This paper focuses on how L. donovani modulates these signaling pathways that favour its survival and persistence in host cells.

摘要

利什曼原虫属的原生动物寄生虫是导致多种被称为利什曼病的人类疾病的原因,这些疾病范围从可自愈的皮肤损伤到内脏器官的严重感染,如果不治疗往往会致命。内脏利什曼病的病原体杜氏利什曼原虫(L. donovani)是一种狡猾的生物体,它已发展出在宿主巨噬细胞内入侵和复制的能力。事实上,这种寄生虫已经进化出策略来干扰巨噬细胞中广泛的信号传导过程,包括蛋白激酶C、JAK2/STAT1级联反应和丝裂原活化蛋白激酶途径。本文重点关注杜氏利什曼原虫如何调节这些有利于其在宿主细胞中存活和持续存在的信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3384/3199940/50ae6d5e14b8/MBI2011-343961.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3384/3199940/50ae6d5e14b8/MBI2011-343961.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3384/3199940/50ae6d5e14b8/MBI2011-343961.001.jpg

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MAPK-directed phosphatases preferentially regulate pro- and anti-inflammatory cytokines in experimental visceral leishmaniasis: involvement of distinct protein kinase C isoforms.MAPK 定向磷酸酶优先调节实验性内脏利什曼病中的促炎和抗炎细胞因子:涉及不同的蛋白激酶 C 同工型。
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Immunology. 2021 Aug;163(4):460-477. doi: 10.1111/imm.13331. Epub 2021 Apr 26.
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Super enhancer-mediated transcription of miR146a-5p drives M2 polarization during Leishmania donovani infection.利什曼原虫感染期间,超级增强子介导的miR146a - 5p转录驱动M2极化。
PLoS Pathog. 2021 Feb 25;17(2):e1009343. doi: 10.1371/journal.ppat.1009343. eCollection 2021 Feb.
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Clin Exp Immunol. 2008 Nov;154(2):224-34. doi: 10.1111/j.1365-2249.2008.03741.x. Epub 2008 Sep 5.
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Identification of leishmania fructose-1,6-bisphosphate aldolase as a novel activator of host macrophage Src homology 2 domain containing protein tyrosine phosphatase SHP-1.鉴定利什曼原虫果糖-1,6-二磷酸醛缩酶为宿主巨噬细胞含Src同源2结构域的蛋白酪氨酸磷酸酶SHP-1的新型激活剂。
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Visceral leishmaniasis - current therapeutic modalities.内脏利什曼病——当前的治疗方式
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Parasitol Res. 2006 Jul;99(2):189-93. doi: 10.1007/s00436-006-0168-1. Epub 2006 Mar 18.