title: The NK2.1 receptor is encoded by Ly-49C and its expression is regulated by MHC class I alleles.
abstract: A dual receptor system composed of activation and inhibitory receptors apparently controls NK cell-mediated lysis. In the C57BL/6 mouse, the NK1.1 molecule acts as an activation receptor whereas Ly-49A, C and G2 can inhibit NK cell lysis of target cells expressing specific MHC class I molecules. We previously reported that NK2.1 is an activation receptor sharing structural properties with members of the NKR-P1 and Ly-49 receptor families. In this study, we have shown that NK2.1 is encoded by the previously described Ly-49C gene. We also found that the expression level of NK2.1/Ly-49C is modulated by H-2-dependent factors and that this regulation differs from that previously described for Ly-49A. Flow cytometry analyses of NK-enriched spleen cells from MHC congenic strains on C57BL/10 and BALB/c backgrounds indeed revealed that the level of NK2.1/Ly-49C expression, but not the number of positive cells, is low in strains expressing H-2b and H-2k haplotypes as compared to H-2d mice. Similar analyses of splenic NK cells from two series of congenic and congenic recombinant strains on the C57BL/10 background indicate that the main regulatory element(s) are most likely the H-2Kb and H-2Dk alleles. Together with our and others previous observations, these results identify the NK2.1/Ly-49C antigen as a receptor for MHC class I molecules whose expression is regulated by host MHC genes.
authors.affiliation: Institut Armand-Frappier, Université du Québec, Laval, Canada.
authors.forename: P
authors.initials: P
authors.lastname: Gosselin
authors.forename: Y
authors.initials: Y
authors.lastname: Lusignan
authors.forename: J
authors.initials: J
authors.lastname: Brennan
authors.forename: F
authors.initials: F
authors.lastname: Takei
authors.forename: S
authors.initials: S
authors.lastname: Lemieux
mesh_terms: D000483:Alleles; D000818:Animals; D000940:Antigenic Variation / Q000276:immunology; D000950:Antigens, Ly / Q000235:genetics*; D015536:Down-Regulation / Q000276:immunology; D005805:Genes, MHC Class I / Q000502:physiology*; D008040:Genetic Linkage; D006183:H-2 Antigens / Q000235:genetics*; D064532:Histocompatibility Antigen H-2D; D007694:Killer Cells, Natural / Q000378:metabolism*; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D008805:Mice, Inbred A; D008806:Mice, Inbred AKR; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D008814:Mice, Inbred NZB; D055650:NK Cell Lectin-Like Receptor Subfamily A; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000235:genetics*; D055630:Receptors, NK Cell Lectin-Like
chemical_list: D000950:Antigens, Ly; D006183:H-2 Antigens; C032876:H-2Kb protein, mouse; D064532:Histocompatibility Antigen H-2D; C527091:Klra3 protein, mouse; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D055650:NK Cell Lectin-Like Receptor Subfamily A; D011971:Receptors, Immunologic; D055630:Receptors, NK Cell Lectin-Like