title: Role of interleukin-12 in determining differential kinetics of invariant natural killer T cells in response to differential burden of Listeria monocytogenes.
abstract: Invariant (i) natural killer (NK) T cells are unique T lymphocytes expressing NKR-P1B/C (NK1.1), which recognize glycolipids, notably alpha-galactosylceramide (alpha-GalCer) presented by CD1d. The characteristic phenotype of these iNKT cells undergoes dramatic changes following Listeria monocytogenes infection, and interleukin (IL)-12 is involved in these alterations. Here we show that liver iNKT cells in mice are differentially influenced by the load of infection. Liver alpha-GalCer/CD1d tetramer-reactive (alpha-GalCer/CD1d(+)) T cells expressing NK1.1 became undetectable by day 2 following L. monocytogenes infection and concomitantly cells lacking NK1.1 increased regardless of the severity of infection. Whereas alpha-GalCer/CD1d(+)NK1.1(+) T cells remained virtually undetectable on day 4 following low-dose infection, considerable numbers of these cells were detected in high-dose-infected mice. Whereas numbers of IL-12 producers in the liver on day 4 post infection were comparable in low- and high-dose-infected mice without in vitro restimulation with heat-killed Listeria, those were more prominent in low-dose-infected mice than in high-dose-infected mice after restimulation despite the fact that higher numbers of macrophages and granulocytes infiltrated the liver in high-dose-infected mice than in low-dose-infected mice. Our results indicate that NK1.1 surface expression on iNKT cells is differentially modulated by the burden of infection, and suggest that a high bacterial load probably causes loss of IL-12 production.
authors.affiliation: Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Emoto
authors.forename: Izumi
authors.initials: I
authors.lastname: Yoshizawa
authors.forename: Robert
authors.initials: R
authors.lastname: Hurwitz
authors.forename: Volker
authors.initials: V
authors.lastname: Brinkmann
authors.forename: Stefan H E
authors.initials: SH
authors.lastname: Kaufmann
authors.forename: Masashi
authors.initials: M
authors.lastname: Emoto
mesh_terms: D000818:Animals; D000950:Antigens, Ly; D000954:Antigens, Surface / Q000378:metabolism; D005260:Female; D054884:Host-Pathogen Interactions; D018664:Interleukin-12 / Q000276:immunology* / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D037181:Lectins, C-Type / Q000378:metabolism; D008089:Listeria monocytogenes / Q000502:physiology; D008088:Listeriosis / Q000276:immunology* / Q000382:microbiology; D008099:Liver / Q000276:immunology; D018655:Lymphocyte Count; D016131:Lymphocyte Subsets; D051379:Mice; D008810:Mice, Inbred C57BL; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011971:Receptors, Immunologic / Q000378:metabolism
chemical_list: D000950:Antigens, Ly; D000954:Antigens, Surface; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011971:Receptors, Immunologic; D018664:Interleukin-12