title: Rapid development of a gamma interferon-secreting glycolipid/CD1d-specific Valpha14+ NK1.1- T-cell subset after bacterial infection.
abstract: The phenotypic and functional changes of glycolipid presented by CD1d(glycolipid/CD1d) specific Valpha14+ T cells in the liver of mice at early stages of bacterial infection were investigated. After Listeria monocytogenes infection or interleukin-12 (IL-12) treatment, alpha-galactosylceramide/CD1d tetramer-reactive (alpha-GalCer/CD1d+) T cells coexpressing natural killer (NK) 1.1 marker became undetectable and, concomitantly, cells lacking NK1.1 emerged in both euthymic and thymectomized animals. Depletion of the NK1.1+ subpopulation prevented the emergence of alpha-GalCer/CD1d+ NK1.1- T cells. Before infection, NK1.1+, rather than NK1.1-, alpha-GalCer/CD1d+ T cells coexpressing CD4 were responsible for IL-4 production, whereas gamma interferon (IFN-gamma) was produced by cells regardless of NK1.1 or CD4 expression. After infection, IL-4-secreting cells became undetectable among alpha-GalCer/CD1d+ T cells, but considerable numbers of IFN-gamma-secreting cells were found among NK1.1-, but not NK1.1+, cells lacking CD4. Thus, NK1.1 surface expression and functional activities of Valpha14+ T cells underwent dramatic changes at early stages of listeriosis, and these alterations progressed in a thymus-independent manner. In mutant mice lacking all alpha-GalCer/CD1d+ T cells listeriosis was ameliorated, suggesting that the subtle contribution of the NK1.1- T-cell subset to antibacterial protection is covered by more profound detrimental effects of the NK1.1+ T-cell subset.
authors.affiliation: Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany. memoto@health.gunma-u.ac.jp
authors.forename: Masashi
authors.initials: M
authors.lastname: Emoto
authors.forename: Izumi
authors.initials: I
authors.lastname: Yoshizawa
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Emoto
authors.forename: Mamiko
authors.initials: M
authors.lastname: Miamoto
authors.forename: Robert
authors.initials: R
authors.lastname: Hurwitz
authors.forename: Stefan H E
authors.initials: SH
authors.lastname: Kaufmann
mesh_terms: D000818:Animals; D018949:Antigens, CD1 / Q000032:analysis; D055610:Antigens, CD1d; D000950:Antigens, Ly; D000954:Antigens, Surface / Q000032:analysis; D005260:Female; D005699:Galactosylceramides / Q000032:analysis; D006017:Glycolipids / Q000032:analysis; D007371:Interferon-gamma / Q000378:metabolism*; D018664:Interleukin-12 / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type / Q000032:analysis; D008089:Listeria monocytogenes; D008088:Listeriosis / Q000276:immunology*; D008099:Liver / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D055651:NK Cell Lectin-Like Receptor Subfamily B; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013950:Thymus Gland / Q000276:immunology
chemical_list: D018949:Antigens, CD1; D055610:Antigens, CD1d; D000950:Antigens, Ly; D000954:Antigens, Surface; D005699:Galactosylceramides; D006017:Glycolipids; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; C493154:alpha-galactosylceramide; D018664:Interleukin-12; D007371:Interferon-gamma