期刊
NATURE IMMUNOLOGY
卷 19, 期 10, 页码 1071-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-018-0203-2
关键词
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类别
资金
- Grant for Joint Research Project of the Institute of Medical Science
- US National Institutes of Health (NIAID) [AI079336]
- University of Tokyo
- Japan Initiative for Global Research Network on Infectious Diseases [JP18fm0108006]
- [16H06388]
- [17H04080]
- [16K08827]
- [17K09369]
- [17K08851]
- [18K07169]
- [17H05069]
- [18K15133]
- [17K19548]
- [17K19549]
- [16H06433]
- [16H06429]
- [16K21723]
- [18H04666]
- [18H04968]
- [18H04856]
TLR3 is a sensor of double-stranded RNA that is indispensable for defense against infection with herpes simplex virus type 1 (HSV-1) in the brain. We found here that TLR3 was required for innate immune responses to HSV-1 in neurons and astrocytes. During infection with HSV-1, TLR3 recruited the metabolic checkpoint kinase complex mTORC2, which led to the induction of chemokines and trafficking of TLR3 to the cell periphery. Such trafficking enabled the activation of molecules (including mTORC1) required for the induction of type I interferons. Intracranial infection of mice with HSV-1 was exacerbated by impairment of TLR3 responses with an inhibitor of mTOR and was significantly 'rescued' by potentiation of TLR3 responses with an agonistic antibody to TLR3. These results suggest that the TLR3-mTORC2 axis might be a therapeutic target through which to combat herpes simplex encephalitis.
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