Autophagy in Tuberculosis

被引：74

作者：

Deretic, Vojo ^{[1
]}

机构：

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

来源：

COLD SPRING HARBOR PERSPECTIVES IN MEDICINE | 2014年 / 4卷 / 11期

基金：

美国国家卫生研究院;

关键词：

MYCOBACTERIUM-TUBERCULOSIS; NONCANONICAL AUTOPHAGY; IL-1-BETA PRODUCTION; CELLULAR AUTOPHAGY; INNATE RESPONSE; RAT-LIVER; PROTEIN; MACROPHAGES; UBIQUITIN; INFECTION;

D O I：

10.1101/cshperspect.a018481

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Autophagy as an immune mechanism controls inflammation and acts as a cell-autonomous defense against intracellular microbes including Mycobacterium tuberculosis. An equally significant role of autophagy is its anti-inflammatory and tissue-sparing function. This combination of antimicrobial and anti-inflammatory actions prevents active disease in animal models. In human populations, genetic links between autophagy, inflammatory bowel disease, and susceptibility to tuberculosis provide further support to these combined roles of autophagy. The autophagic control of M. tuberculosis and prevention of progressive disease provide novel insights into physiological and immune control of tuberculosis. It also offers host-based therapeutic opportunities because autophagy can be pharmacologically modulated.

引用

页数：15

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