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杀戮:模型系统能教给我们什么。

Killing : What Model Systems Can Teach Us.

机构信息

Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461.

Department of Microbiology and Immunology, Oregon Health Sciences University, Portland OR, 97239.

出版信息

Microbiol Spectr. 2017 Jun;5(3). doi: 10.1128/microbiolspec.TBTB2-0028-2016.

Abstract

Tuberculosis is one of the most successful human diseases in our history due in large part to the multitude of virulence factors exhibited by the causative agent, . Understanding the pathogenic nuances of this organism in the context of its human host is an ongoing topic of study facilitated by isolating cells from model organisms such as mice and non-human primates. However, is an obligate intracellular human pathogen, and disease progression and outcome in these model systems can differ from that of human disease. Current models of infection include primary macrophages and macrophage-like immortalized cell lines as well as the induced pluripotent stem cell-derived cell types. This article will discuss these model systems in general, what we have learned so far about utilizing them to answer questions about pathogenesis, the potential role of other cell types in innate control of infection, and the development of new coculture systems with multiple cell types. As we continue to expand current systems and institute new ones, the knowledge gained will improve our understanding of not only tuberculosis but all infectious diseases.

摘要

结核病是人类历史上最成功的疾病之一,这在很大程度上要归功于病原体表现出的多种毒力因子。了解该生物体在人类宿主中的致病细微差别是一个正在进行的研究课题,其方法是从模型生物(如小鼠和非人类灵长类动物)中分离细胞。然而, 是一种必需的人体细胞内病原体,这些模型系统中的疾病进展和结果可能与人类疾病不同。目前的 感染模型包括原代巨噬细胞和巨噬细胞样永生化细胞系以及诱导多能干细胞衍生的细胞类型。本文将一般性地讨论这些 模型系统,迄今为止我们利用它们来回答关于发病机制的问题所学到的知识,其他细胞类型在固有控制 感染中的潜在作用,以及开发具有多种细胞类型的新共培养系统。随着我们继续扩展当前的 系统并引入新的系统,所获得的知识将不仅提高我们对结核病的理解,而且提高我们对所有传染病的理解。

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本文引用的文献

1
Innate Immunity Holding the Flanks until Reinforced by Adaptive Immunity against Mycobacterium tuberculosis Infection.
Front Microbiol. 2016 Mar 14;7:328. doi: 10.3389/fmicb.2016.00328. eCollection 2016.
2
A Locus at 5q33.3 Confers Resistance to Tuberculosis in Highly Susceptible Individuals.
Am J Hum Genet. 2016 Mar 3;98(3):514-524. doi: 10.1016/j.ajhg.2016.01.015.
4
Mouse models of human TB pathology: roles in the analysis of necrosis and the development of host-directed therapies.
Semin Immunopathol. 2016 Mar;38(2):221-37. doi: 10.1007/s00281-015-0538-9. Epub 2015 Nov 5.
5
The tuberculosis necrotizing toxin kills macrophages by hydrolyzing NAD.
Nat Struct Mol Biol. 2015 Sep;22(9):672-8. doi: 10.1038/nsmb.3064. Epub 2015 Aug 3.
6
Essential roles of methionine and S-adenosylmethionine in the autarkic lifestyle of Mycobacterium tuberculosis.
Proc Natl Acad Sci U S A. 2015 Aug 11;112(32):10008-13. doi: 10.1073/pnas.1513033112. Epub 2015 Jul 28.
7
The Cytosolic Sensor cGAS Detects Mycobacterium tuberculosis DNA to Induce Type I Interferons and Activate Autophagy.
Cell Host Microbe. 2015 Jun 10;17(6):811-819. doi: 10.1016/j.chom.2015.05.004. Epub 2015 Jun 2.
8
Immunoevasion and immunosuppression of the macrophage by Mycobacterium tuberculosis.
Immunol Rev. 2015 Mar;264(1):220-32. doi: 10.1111/imr.12268.
10
Immunology studies in non-human primate models of tuberculosis.
Immunol Rev. 2015 Mar;264(1):60-73. doi: 10.1111/imr.12258.

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