title: High expression of NK-1.1 antigen is induced by infection with murine AIDS virus.
abstract: Spleen cells from mice infected with LP-BM5 MuLV, a causative agent of murine acquired immunodeficiency syndrome (MAIDS), were tested for frequency of NK-1.1+ cells and natural killer (NK) activity. During the first 3 weeks following infection, NK activity was well conserved, but by 9-12 weeks post-infection (p.i.), killer activity was depressed; however, the frequency of NK-1.1+ cells increased within 4 weeks of infection and remained elevated thereafter, even following the decline in functional killing activity. Since the absolute number of NK-1.1+ cells increased after infection, the ability of each NK-1.1+ cell to kill the targets seems drastically impaired. Extraordinary expansion of NK-1.1-positive cells was induced by infection with LP-BM5-defective virus (BM5def), a crucial element for MAIDS induction, but not with a helper non-pathogenic virus. With advance of MAIDS the NK-1.1 antigen (Ag) was preferentially expressed on B220+ and Thy-1+ cells, in contrast to CD4+ and CD8+ cells, and among activated large cells a higher proportion was NK-1.1+ than NK-1.1-. Mice with graft-versus-host disease (GVHD) due to class II major histocompatibility complex (MHC) Ag disparity showed a high frequency of NK-1.1 expression in association with other phenotypic alterations, very similar to those seen in mice with MAIDS. In contrast, B6-lpr/lpr mice developed similar activation of B cells but did not exhibit enhanced expression of the NK-1.1 marker. Thus, enhanced expression of the NK-1.1 Ag might be associated with chronic activation of lymphocytes through a common but not universal pathway.
authors.affiliation: Department of Bacterial and Blood Products, National Institutes of Health, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Makino
authors.forename: D F
authors.initials: DF
authors.lastname: Winkler
authors.forename: J
authors.initials: J
authors.lastname: Wunderlich
authors.forename: J W
authors.initials: JW
authors.lastname: Hartley
authors.forename: H C
authors.initials: HC
authors.lastname: Morse
authors.forename: K L
authors.initials: KL
authors.lastname: Holmes
mesh_terms: D000818:Animals; D000941:Antigens / Q000032:analysis*; D000950:Antigens, Ly; D000954:Antigens, Surface / Q000032:analysis; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D005260:Female; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type; D008198:Lymph Nodes / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology*; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins / Q000032:analysis*; D013154:Spleen / Q000276:immunology
chemical_list: D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins