Mycobacterium tuberculosis effectors interfering host apoptosis signaling
Mycobacterium tuberculosis effectors interfering host apoptosis signaling
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DOI：
10.1007/s10495-015-1115-3
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发表时间：
2015-07-01
期刊：
影响因子：
7.2
通讯作者：
Xie, Jianping
中科院分区：
文献类型：
--
作者：
Liu, Minqiang;Li, Wu;Xie, Jianping
结核病仍然是一个严重的人类公共卫生问题。其病原体结核分枝杆菌与人类宿主之间的共同进化使结核病的预防和治疗方法变得复杂。细胞凋亡在这种相互作用中起着微妙的作用。病原体试图通过针对关键信号节点的多种效应物来调控细胞凋亡。在本文中，我们总结了病原体用于破坏细胞凋亡的效应物，如LpqH、ESAT - 6/CFP - 10、脂阿拉伯甘露聚糖（LAMs）。还讨论了不同形式的细胞死亡（如细胞凋亡、自噬、坏死）之间的相互作用，重点关注效应物的作用方式以及对更好地控制结核病的意义。
Tuberculosis remains a serious human public health concern. The coevolution between its pathogen Mycobacterium tuberculosis and human host complicated the way to prevent and cure TB. Apoptosis plays subtle role in this interaction. The pathogen endeavors to manipulate the apoptosis via diverse effectors targeting key signaling nodes. In this paper, we summarized the effectors pathogen used to subvert the apoptosis, such as LpqH, ESAT-6/CFP-10, LAMs. The interplay between different forms of cell deaths, such as apoptosis, autophagy, necrosis, is also discussed with a focus on the modes of action of effectors, and implications for better TB control.