title: Predominant appearance of NK1.1+ T cells producing IL-4 may be involved in the increased susceptibility of mice with the beige mutation during Salmonella infection.
abstract: C57BL/6 mice with the beige mutation (beige mice) showed a high susceptibility to infection with Salmonella choleraesuis compared with C57BL/6 (B6) control mice, as assessed by bacterial number in the peritoneal cavity and the liver. The appearance of NK1.1+ CD3- NK cells was significantly suppressed, while NK1.1+ T cells were increased in the peritoneal cavity of beige mice after Salmonella infection. The expression level of IL-4 mRNA was much higher in freshly isolated NK1.1+ T cells of the infected beige mice, but the expression level of IFN-gamma mRNA was lower than that in the infected control mice. The NK1.1+ T cells produced more IL-4 in response to TCR alphabeta cross-linking, whereas IFN-gamma production upon TCR triggering was significantly impaired in the beige mice compared to that in the control mice. Furthermore, the generation of Salmonella-specific Th1 cells producing IFN-gamma was significantly inhibited in the peritoneal cavity of beige mice after Salmonella infection. However, administration of anti-IL-4 neutralizing mAb to beige mice during salmonellosis restored the generation of Salmonella-specific Th1 cells and decreased the susceptibility to Salmonella. These results suggested that the predominant activation of NK1.1+ T cells producing IL-4 over those producing IFN-gamma may be at least partly involved in the poor generation of Salmonella-specific protective Th1 cells, resulting in the increased susceptibility of beige mice to Salmonella infection.
authors.affiliation: Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Enomoto
authors.forename: H
authors.initials: H
authors.lastname: Nishimura
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshikai
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex; D004198:Disease Susceptibility; D005260:Female; D016130:Immunophenotyping; D007274:Injections, Intraperitoneal; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis* / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010529:Peritoneal Cavity / Q000166:cytology; D011506:Proteins; D012333:RNA, Messenger / Q000096:biosynthesis; D012481:Salmonella Infections, Animal / Q000235:genetics* / Q000276:immunology* / Q000517:prevention & control; D016176:T-Lymphocyte Subsets / Q000145:classification / Q000276:immunology* / Q000378:metabolism*; D018417:Th1 Cells / Q000276:immunology / Q000382:microbiology
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D012333:RNA, Messenger; D018664:Interleukin-12; D015847:Interleukin-4