期刊
VACCINES
卷 8, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/vaccines8010142
关键词
enforced replication; vaccination; innate immunity; adaptive immunity; CD169(+) macrophages; Usp18; Ebola virus; VSV-EBOV; Ervebo
资金
- Deutsche Forschungsgemeinschaft (DFG) [LA1419/7-1, LA1419/10-1, LA1558/5-1, SI1558/3-1]
- University of Duisburg-Essen
- [Sonderforschungsbereich SFB974]
- [Transregio TRR60]
- [RTG1949]
- [RTG2098]
Ebola virus epidemics can be effectively limited by the VSV-EBOV vaccine (Ervebo) due to its rapid protection abilities; however, side effects prevent the broad use of VSV-EBOV as vaccine. Mechanisms explaining the efficient immune activation after single injection with the VSV-EBOV vaccine remain mainly unknown. Here, using the clinically available VSV-EBOV vaccine (Ervebo), we show that the cell-intrinsic expression of the interferon-inhibitor Usp18 in CD169(+) macrophages is one important factor modulating the anti-Ebola virus immune response. The absence of Usp18 in CD169(+) macrophages led to the reduced local replication of VSV-EBOV followed by a diminished innate as well as adaptive immune response. In line, CD169-Cre(+/ki) x Usp18(fl/fl) mice showed reduced innate and adaptive immune responses against the VSV wildtype strain and died quickly after infection, suggesting that a lack of Usp18 makes mice more susceptible to the side effects of the VSV vector. In conclusion, our study shows that Usp18 expression in CD169(+) macrophages is one important surrogate marker for effective vaccination against VSV-EBOV, and probably other VSV-based vaccines also.
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