Abstract
Abstract NK cells have the capacity to efficiently kill tumor cells. NK cells will be triggered to do so upon loss of MHC class I expression on the tumor cells, that is missing-self recognition. However, not all NK cells in an individual are able to perform such missing-self responses. The ability to perform missing-self is acquired through a process of education where only NK cells with an ability to interact with MHC class I are allowed full functionality. We have recently shown that this NK cell education is not a binary but a quantitative process, yielding NK cells that are more or less efficient killers depending on the strength of interaction with self MHC class I during education (Brodin et al Blood 2009). Here we describe our latest unpublished results on the MHC class I medicated influence on the NK cell system in the mouse. We show that MHC class I not only controls function but also NK cell population dynamics leading to a repertoire of NK cells that differ between individuals in a MHC class I dependent way. Combined these MHC class I mediated effects control the ability of an individual to perform missing-self responses cells lacking MHC class I in vivo. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr B54.
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