期刊
CELLULAR & MOLECULAR IMMUNOLOGY
卷 17, 期 9, 页码 901-913出版社
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/s41423-020-0502-z
关键词
Mycobacterium tuberculosis; Innate immunity; Innate immune receptors; Autophagy; Ubiquitin system
类别
资金
- National Key Research and Development Program of China [2017YFA0505900]
- National Natural Science Foundation of China [81825014, 31830003, 91842303, 31730025, 81330069]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB29020000]
- Key Program of Logistics Research [BWS17J030]
- Shanghai Municipal Education Commission
- Shanghai Education Development Foundation [19CG22]
Mycobacterium tuberculosis(Mtb) is an extremely successful intracellular pathogen that causes tuberculosis (TB), which remains the leading infectious cause of human death. The early interactions between Mtb and the host innate immune system largely determine the establishment of TB infection and disease development. Upon infection, host cells detect Mtb through a set of innate immune receptors and launch a range of cellular innate immune events. However, these innate defense mechanisms are extensively modulated by Mtb to avoid host immune clearance. In this review, we describe the emerging role of cytosolic nucleic acid-sensing pathways at the host-Mtb interface and summarize recently revealed mechanisms by which Mtb circumvents host cellular innate immune strategies such as membrane trafficking and integrity, cell death and autophagy. In addition, we discuss the newly elucidated strategies by which Mtb manipulates the host molecular regulatory machinery of innate immunity, including the intranuclear regulatory machinery, the ubiquitin system, and cellular intrinsic immune components. A better understanding of innate immune evasion mechanisms adopted by Mtb will provide new insights into TB pathogenesis and contribute to the development of more effective TB vaccines and therapies.
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