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- W4313360000 abstract "Abstract Natural Killer (NK) cells are innate lymphocytes involved in anti-viral and anti-cancer responses. They can be functionally and phenotypically divided based on expression of inhibitory receptors capable of binding to self-MHC class I, a concept termed licensing/education. NK cells capable of binding to self-MHC (licensed) have been shown to be more functionally competent compared to those that cannot (unlicensed). It is still unclear which subset is more critical during an anti-viral response. Using two models of murine cytomegalovirus infection (MCMV), we show distinct subsets of NK cells that can both directly and indirectly contribute to the anti-viral response. We have previously shown that after hematopoietic stem cell transplantation (HSCT), the licensed effector NK population was predominantly responsible for resistance to MCMV, which was in part due to the absence of T cells present immediately after transplant. However, MCMV infection in non-HSCT mice yielded an opposite pattern with the unlicensed NK subset augmenting resistance to MCMV. We found preferential localization patterns of the different NK subsets which correlated with increased antigen specific T cell expansion and viral clearance. Interestingly, by depleting the different NK subsets in HSCT vs non-HSCT mice, we demonstrated differences in subset roles. The unlicensed NK cells, which promote antigen specific T cells, are more critical during normal conditions, while the licensed NK cells serve a better direct anti-viral role following HSCT where T cells take longer to repopulate. Thus, the contributions of these different NK subsets and their dependence on the immune environment should be taken into consideration when applying NK cells therapeutically." @default.
- W4313360000 created "2023-01-06" @default.
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- W4313360000 date "2017-05-01" @default.
- W4313360000 modified "2023-10-16" @default.
- W4313360000 title "The immune environment dictates the dominance of licensed versus unlicensed natural killer cell subsets during viral infection" @default.
- W4313360000 doi "https://doi.org/10.4049/jimmunol.198.supp.68.18" @default.
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