title: Stringent V beta requirement for the development of NK1.1+ T cell receptor-alpha/beta+ cells in mouse liver.
abstract: The liver of C57BL/6 mice contains a major subset of CD4+8- and CD4-8- T cell receptor (TCR)-alpha/beta+ cells expressing the polymorphic natural killer NK1.1 surface marker. Liver NK1.1+TCR-alpha/beta+ (NK1+ T) cells require interaction with beta2-microglobulin-associated, major histocompatibility complex I-like molecules on hematopoietic cells for their development and have a TCR repertoire that is highly skewed to Vbeta8.2, Vbeta7, and Vbeta2. We show here that congenic C57BL/6.Vbeta(a) mice, which lack Vbeta8- expressing T cells owing to a genomic deletion at the Vbeta locus, maintain normal levels of liver NK1+ T cells owing to a dramatic increase in the proportion of cells expressing Vbeta7 and Vbeta2 (but not other Vbetas). Moreover, in C57BL/6 congenic TCR-V Vbeta3 and -Vbeta8.1 transgenic mice (which in theory should not express other Vbeta, owing to allelic exclusion at the TCR-beta locus), endogenous TCR-Vbeta8.2, Vbeta7, and Vbeta2 (but not other Vbetas) are frequently expressed on liver NK1+T cells but absent on lymph node T cells. Finally, when endogenous V beta expression is prevented in TCR-Vbeta3 and Vbeta8.1 transgenic mice (by introduction of a null allele at the C beta locus), the development of liver NK1+T cells is totally abrogated. Collectively, our data indicate that liver NK1+T cells have a stringent requirement for expression of TCR-Vbeta8.2, Vbeta7, or Vbeta2 for their development.
authors.affiliation: Ludwig Institute for Cancer Research, University of Lausanne, Switzerland.
authors.forename: T
authors.initials: T
authors.lastname: Ohteki
authors.forename: H R
authors.initials: HR
authors.lastname: MacDonald
mesh_terms: D000483:Alleles; D000818:Animals; D000941:Antigens / Q000096:biosynthesis* / Q000235:genetics; D000950:Antigens, Ly; D000954:Antigens, Surface; D015704:CD4 Antigens / Q000276:immunology; D005434:Flow Cytometry; D006239:Haplotypes; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type; D008099:Liver / Q000276:immunology*; D008198:Lymph Nodes / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D055651:NK Cell Lectin-Like Receptor Subfamily B; D009928:Organ Specificity; D011110:Polymorphism, Genetic; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000096:biosynthesis* / Q000235:genetics; D017384:Sequence Deletion; D016176:T-Lymphocyte Subsets / Q000276:immunology; D001613:beta 2-Microglobulin / Q000276:immunology
chemical_list: D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D015704:CD4 Antigens; D015395:Histocompatibility Antigens Class I; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D001613:beta 2-Microglobulin