title: Reversible NK1.1 surface expression on invariant liver natural killer T cells during Listeria monocytogenes infection.
abstract: The invariant (i) natural killer (NK)T cells consistently express the Valpha14 chain of the T cell receptor (TCR) and recognize alpha-galactosylceramide (alpha-GalCer) presented by the nonpolymorphic presentation molecule CD1d. Despite their name, the iNKT cells represent a heterogeneous population, which can be divided on the basis of NK1.1 surface expression. Here we show that NK1.1 surface expression on liver iNKT cells in mice fluctuates during Listeria monocytogenes infection. At early stages of listeriosis, iNKT cells expressing NK1.1 were numerically reduced and those lacking NK1.1 were increased. At later time points, the NK1.1(-) iNKT cell population contracted, whereas NK1.1(+) iNKT cells reemerged. Alterations in NK1.1 surface expression on iNKT cells were paralleled by numerical changes of interleukin (IL)-12 producers in the liver and were completely prevented by endogenous IL-12 neutralization, whereas NK1.1 surface alterations on iNKT cells following alpha-GalCer stimulation were not prevented. Adoptive cell transfer experiments revealed that the liver NK1.1(-) iNKT cells from NK1.1(+) cell-depleted L. monocytogenes-infected mice accumulated in the liver of recipient recombination-activating gene-1-deficient mice where they acquired NK1.1 surface expression. Thus, we present first evidence that NK1.1 surface expression on liver iNKT cells is reversible during L. monocytogenes infection, and that different mechanisms underlie stimulation by TCR and IL-12.
authors.affiliation: Department of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117 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: Yusuke
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Robert
authors.initials: R
authors.lastname: Hurwitz
authors.forename: Mamiko
authors.initials: M
authors.lastname: Miamoto
authors.forename: Stefan H E
authors.initials: SH
authors.lastname: Kaufmann
mesh_terms: D000818:Animals; D018949:Antigens, CD1 / Q000378:metabolism; D055610:Antigens, CD1d; D000950:Antigens, Ly; D000954:Antigens, Surface / Q000378:metabolism*; D005260:Female; D005699:Galactosylceramides / Q000378:metabolism; D018664:Interleukin-12; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type / Q000378:metabolism*; D008089:Listeria monocytogenes; D008088:Listeriosis / Q000276:immunology / Q000382:microbiology; D008099:Liver / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D055651:NK Cell Lectin-Like Receptor Subfamily B
chemical_list: D018949:Antigens, CD1; D055610:Antigens, CD1d; D000950:Antigens, Ly; D000954:Antigens, Surface; D005699:Galactosylceramides; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; C493154:alpha-galactosylceramide; D018664:Interleukin-12