Immune evasion and provocation by Mycobacterium tuberculosis

被引:239
作者
Chandra, Pallavi [1 ,2 ]
Grigsby, Steven J. [1 ,2 ]
Philips, Jennifer A. [1 ,2 ]
机构
[1] Washington Univ, Sch Med, Dept Med, Div Infect Dis, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
CD4; T-CELLS; HEMATOPOIETIC STEM-CELLS; HOST-DIRECTED THERAPY; ALVEOLAR MACROPHAGES; INNATE IMMUNITY; SUCCINATE-DEHYDROGENASE; GRANULOMA-FORMATION; NLRP3; INFLAMMASOME; BACTERIAL-GROWTH; DENDRITIC CELLS;
D O I
10.1038/s41579-022-00763-4
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
In this Review, Chandra, Grigsby and Philips discuss how Mycobacterium tuberculosis evades immune-mediated clearance while capitalizing on the host inflammatory response at different phases of its life cycle. They focus on recent studies, highlight gaps in knowledge and consider how our current understanding will inform new therapies, vaccines and diagnostics. Mycobacterium tuberculosis, the causative agent of tuberculosis, has infected humans for millennia. M. tuberculosis is well adapted to establish infection, persist in the face of the host immune response and be transmitted to uninfected individuals. Its ability to complete this infection cycle depends on it both evading and taking advantage of host immune responses. The outcome of M. tuberculosis infection is often a state of equilibrium characterized by immunological control and bacterial persistence. Recent data have highlighted the diverse cell populations that respond to M. tuberculosis infection and the dynamic changes in the cellular and intracellular niches of M. tuberculosis during the course of infection. M. tuberculosis possesses an arsenal of protein and lipid effectors that influence macrophage functions and inflammatory responses; however, our understanding of the role that specific bacterial virulence factors play in the context of diverse cellular reservoirs and distinct infection stages is limited. In this Review, we discuss immune evasion and provocation by M. tuberculosis during its infection cycle and describe how a more detailed molecular understanding is crucial to enable the development of novel host-directed therapies, disease biomarkers and effective vaccines.
引用
收藏
页码:750 / 766
页数:17
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