期刊
NATURE IMMUNOLOGY
卷 11, 期 10, 页码 912-U61出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1933
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资金
- National Institutes of Health [AI-055749, AI-50031]
- Howard Hughes Medical Institute
- Northeast Biodefense Center [U54-AI057158-Lipkin]
- Canadian Institutes for Health Research [79410]
Caspase-12 has been shown to negatively modulate inflammasome signaling during bacterial infection. Its function in viral immunity, however, has not been characterized. We now report an important role for caspase-12 in controlling viral infection via the pattern-recognition receptor RIG-I. After challenge with West Nile virus (WNV), caspase-12-deficient mice had greater mortality, higher viral burden and defective type I interferon response compared with those of challenged wild-type mice. In vitro studies of primary neurons and mouse embryonic fibroblasts showed that caspase-12 positively modulated the production of type I interferon by regulating E3 ubiquitin ligase TRIM25-mediated ubiquitination of RIG-I, a critical signaling event for the type I interferon response to WNV and other important viral pathogens.
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