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- W161539441 abstract "Natural Killer (NK) cell functionality is controlled by inhibitory receptors that recognize self-MHC class I. NK cells that do not interact with self-MHC class I are hypo-responsive to many stimuli and fail to reject MHC class I-deficient cells. Thus, although the mechanisms are unknown, interactions with MHC class I “licensed” NK cells respond efficiently. Surprisingly, these licensed NK cells fail to control viral infection. During mouse cytomegalovirus (MCMV) infection, SHP-1 signaling downstream of inhibitory receptors for MHC class I limits NK cell proliferation. Interactions with MHC class I prevent licensed NK cells from controlling of MCMV replication and pathogenesis; rather, it is the unlicensed NK cells that are not inhibited by self-MHC class I that efficiently control MCMV infection. Therefore, the licensing hypothesis is not sufficient to explain NK cell functionality during viral infection." @default.
- W161539441 created "2016-06-24" @default.
- W161539441 creator A5000763253 @default.
- W161539441 creator A5064743187 @default.
- W161539441 date "2011-01-01" @default.
- W161539441 modified "2023-10-16" @default.
- W161539441 title "Natural Killer Cell Licensing During Viral Infection" @default.
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- W161539441 doi "https://doi.org/10.1007/978-1-4419-5632-3_4" @default.
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