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Immune evasion and provocation by Mycobacterium tuberculosis
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 depe...
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Published in: | Nature reviews. Microbiology 2022-12, Vol.20 (12), p.750-766 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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.
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. |
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ISSN: | 1740-1526 1740-1534 1740-1534 |
DOI: | 10.1038/s41579-022-00763-4 |