Autophagy as an immune effector against tuberculosis.

Autophagy as an immune effector against tuberculosis.
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DOI:
10.1016/j.mib.2013.05.003
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发表时间:
2013-06
影响因子:
5.4
通讯作者:
Deretic V
Deretic V
中科院分区:
生物学2区
文献类型:
--
作者:
Bradfute SB;Castillo EF;Arko-Mensah J;Chauhan S;Jiang S;Mandell M;Deretic V

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现在被广泛接受的先天免疫范式是自噬作为细胞内细菌的细胞自主防御,其关键起源是对结核分枝杆菌的研究,结核分枝杆菌是一种重要的人类病原体和感染巨噬细胞的模式微生物。已经确定了许多不同的因素在自噬的抗分枝杆菌功能中起作用,最近在小鼠结核病模型中的体内研究发现了自噬的其他抗炎和组织保存功能。与这些观察结果相补充的是,全基因组关联研究表明,自噬、人类对分枝杆菌感染的易感性和炎症性肠病易感性位点之间存在相当大的重叠。最后,最近的研究表明,自噬是IL-1反应的重要调节者和效应者,并且自噬与I型干扰素病理调节反应交叉。
The now well-accepted innate immunity paradigm that autophagy acts as a cell-autonomous defense against intracellular bacteria has its key origins in studies with Mycobacterium tuberculosis, an important human pathogen and a model microorganism infecting macrophages. A number of different factors have been identified that play into the anti-mycobacterial functions of autophagy, and recent in vivo studies in the mouse model of tuberculosis have uncovered additional anti-inflammatory and tissue-sparing functions of autophagy. Complementing these observations, genome wide association studies indicate a considerable overlap between autophagy, human susceptibility to mycobacterial infections, and predisposition loci for inflammatory bowel disease. Finally, recent studies show that autophagy is an important regulator and effector of IL-1 responses, and that autophagy intersects with type I interferon pathology-modulating responses.
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期刊: Science (New York, N.Y.)
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