期刊
FEMS MICROBIOLOGY REVIEWS
卷 36, 期 3, 页码 514-532出版社
OXFORD UNIV PRESS
DOI: 10.1111/j.1574-6976.2012.00331.x
关键词
granuloma; persistence; host immune response; latency
类别
资金
- European 7th Framework Program SYSTEMTB [HEALTH-2009-2.1.2-1-241587]
- National Institutes of Health (SysBio) [745090 HHSN272200800059C]
Tuberculosis (TB) remains a major health threat, killing nearly 2 million individuals around this globe, annually. The only vaccine, developed almost a century ago, provides limited protection only during childhood. After decades without the introduction of new antibiotics, several candidates are currently undergoing clinical investigation. Curing TB requires prolonged combination of chemotherapy with several drugs. Moreover, monitoring the success of therapy is questionable owing to the lack of reliable biomarkers. To substantially improve the situation, a detailed understanding of the cross-talk between human host and the pathogen Mycobacterium tuberculosis (Mtb) is vital. Principally, the enormous success of Mtb is based on three capacities: first, reprogramming of macrophages after primary infection/phagocytosis to prevent its own destruction; second, initiating the formation of well-organized granulomas, comprising different immune cells to create a confined environment for the hostpathogen standoff; third, the capability to shut down its own central metabolism, terminate replication, and thereby transit into a stage of dormancy rendering itself extremely resistant to host defense and drug treatment. Here, we review the molecular mechanisms underlying these processes, draw conclusions in a working model of mycobacterial dormancy, and highlight gaps in our understanding to be addressed in future research.
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