Autophagy as an immune effector against tuberculosis

被引：91

作者：

Bradfute, Steven B. ^{[1
]}

Castillo, Eliseo F. ^{[1
]}

Arko-Mensah, John ^{[1
]}

Chauhan, Santosh ^{[1
]}

Jiang, Shanya ^{[1
]}

Mandell, Michael ^{[1
]}

Deretic, Vojo ^{[1
]}

机构：

[1] Univ New Mexico, Dept Mol Genet & Microbiol, Hlth Sci Ctr, Albuquerque, NM 87131 USA

来源：

CURRENT OPINION IN MICROBIOLOGY | 2013年 / 16卷 / 03期

关键词：

CYCLIC GMP-AMP; MYCOBACTERIUM-TUBERCULOSIS; IL-1-BETA PRODUCTION; INNATE RESPONSE; RECEPTOR NDP52; IFN-GAMMA; PROTEIN; INFECTION; PATHWAY; MACROPHAGES;

D O I：

10.1016/j.mib.2013.05.003

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

引用

页码：355 / 365

页数：11

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