期刊
IMMUNITY
卷 40, 期 6, 页码 949-960出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.05.004
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资金
- Alexander von Humboldt Foundation [SKA2008, SKA2010]
- German Research Council [SFB974, LA2558/3-1, LA2558/5-1, TRR60, LA1419/5-1, RTG1949]
- NIH Tetramer Facility
- Strategic Research Fund
- Forschungskomission of the Heinrich Heine University
Despite development of new antiviral drugs, viral infections are still a major health problem. The most potent antiviral defense mechanism is the innate production of type I interferon (IFN-I), which not only limits virus replication but also promotes antiviral T cell immunity through mechanisms, which remain insufficiently studied. Using the murine lymphocytic choriomeningitis virus model system, we show here that IFN-I signaling on T cells prevented their rapid elimination in vivo. Microarray analyses uncovered that IFN-I triggered the expression of selected inhibitory NK-cell-receptor ligands. Consequently, T cell immunity of IFN-I receptor (IFNAR)-deficient T cells could be restored by NK cell depletion or in NK-cell-deficient hosts (Nfil3(-/-)).The elimination of Ifnar1(-/-) T cells was dependent on NK-cell-mediated perforin expression. In summary, we identified IFN-I as a key player regulating the protection of T cells against regulatory NK cell function.
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