期刊
CELLULAR & MOLECULAR IMMUNOLOGY
卷 14, 期 12, 页码 963-975出版社
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/cmi.2017.88
关键词
host-pathogen interactions; immune evasion; innate immune defense; Mycobacterium tuberculosis; tuberculosis
类别
资金
- National Key Research and Development Program of China [2017YFA0505900, 2017YFD0500300]
- National Basic Research Programs of China [2014CB74440]
- National Natural Science Foundation of China [81371769, 81571954]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDPB03]
- Youth Innovation Promotion Association CAS [Y12A027BB2]
The major innate immune cell types involved in tuberculosis (TB) infection are macrophages, dendritic cells (DCs), neutrophils and natural killer (NK) cells. These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis (Mtb) through various pattern recognition receptors (PRRs), including but not limited to Toll-like receptors (TLRs), Nod-like receptors (NLRs) and C-type lectin receptors (CLRs). Upon infection by Mtb, the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis, autophagy, apoptosis and inflammasome activation. In contrast, Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity. Here we discuss recent research on major host innate immune cells, PRR signaling, and the cellular functions involved in Mtb infection, with a specific focus on the host's innate immune defense and Mtb immune evasion. A better understanding of the molecular mechanisms underlying host-pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.
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