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*
Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden;
Department of Immunology, Microbiology, Pathology, and Infectious Diseases, Karolinska Institute, Huddinge University Hospital, Huddinge, Sweden;
Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden; and
§
Centre de Recherche en Immunologie, Institut Armand-Frappier, Université du Québec, Laval, Quebec, Canada
We have analyzed lymphocyte development in natural MHC class I chimeric mice, generated through a transgenic approach in ß2-microglobulin (ß2m)-/- mice. In these mice, MHC class I+ cells coexist with an equal proportion of MHC class I-deficient cells. These MHC class I mosaic mice had normal numbers of CD8+ T cells, which had a target cell specificity similar to that of wild-type mice. Consequently, the mice did not develop any signs of autoimmunity. They also had normal numbers of NK cells. This allowed an examination of the MHC class I influence on the expression of the Ly49C inhibitory receptor on NK cells. This receptor binds to H-2Kb. It is expressed at low levels on NK cells in wild-type mice of the H-2b haplotype, but at markedly higher levels on NK cells in ß2m-/- mice and other strains of mice lacking expression of H-2Kb. Relatively little is known about how MHC class I molecules affect expression of the Ly49 receptors. Through the analysis of the present MHC class I mosaic mice, we demonstrate that the expression levels of Ly49C on NK cells is a consequence not only of MHC class I expression in the environment, but also of the expression of MHC class I molecules by the NK cells themselves. These findings are discussed in relation to the biological role of the calibration of the Ly49 inhibitory receptor expression in relation to self-MHC class I.
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