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NK Cells from Human MHC Class I (HLA-B) Transgenic Mice Do Not Mediate Hybrid Resistance Killing Against Parental Nontransgenic cells¹

Sam K. P. Kung^*, Ruey-Chyi Su^*, Jeremy J. K. Graham, John W. Chamberlain and Richard G. Miller^2,*

^* Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, Toronto, Canada; and Research Institute, The Hospital of Sick Children, and Department of Immunology, University of Toronto, Toronto, Canada

We have investigated the capacity of human MHC class I HLA-B gene products, HLA-B27, -B7 (fully human), and -B7K^b (human-mouse hybrid consisting of the 1 and 2 domains of HLA-B7, and the 3 and cytoplasmic domains of mouse H-2K^b), expressed on mouse NK cells during ontogeny to influence NK recognition of otherwise syngeneic mouse target cells. Despite a high level of surface expression of the transgene (comparable to that of endogeneous H-2D^bK^b molecules), the direct killing of YAC-1 targets, and the killing of P815 targets in a redirected lysis assay, the NK effectors of these transgenic mice could not mediate hybrid resistance-like killing of nontransgenic C57BL/6 target cells either in vitro or in vivo. Splenocytes from B6-B27 mice could be used to generate CTL lines against a B27-binding peptide, implying that T cells restricted by HLA-B27 developed during ontogeny. NK cells from B6-B27 could lyse B6-B27 Con A lymphoblasts pulsed with D^b-binding peptide but not B27-binding peptides. Taken together, our results show that these human HLA-B transgene products cannot function as class I MHC "self" elements for mouse NK cells, even when present throughout ontogeny.

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