title: Expansion and function of CD8+ T cells expressing Ly49 inhibitory receptors specific for MHC class I molecules.
abstract: MHC class I-specific Ly49 inhibitory receptors regulate NK cell activation, thereby preventing autologous damage to normal cells. Ly49 receptors are also expressed on a subset of CD8+ T cells whose origin and function remain unknown. We report here that, despite their phenotypic and cytolytic similarities, Ly49+CD8+ T cells and conventional Ly49-CD44high memory-phenotype CD8+ T cells present strikingly distinct features. First, under steady state conditions Ly49+CD8+ T cells are poor cytokine producers (TNF-alpha and IFN-gamma) upon TCR triggering. Second, Ly49+CD8+ T cells are not induced upon various settings of Ag immunization or microbial challenge. However, Ly49 can be induced on a fraction of self-specific CD8+ T cells if CD4+ T cells are present. Finally, the size of the Ly49+CD8+ T cell subset is selectively reduced in the absence of STAT1. These results indicate that Ly49 expression is associated with a differentiation program of cytolytic CD8+ T cells triggered upon chronic antigenic exposure. They further suggest that the size of the Ly49+CD8+ T cell subset marks a history of CD8+ T cell activation that might preferentially result from endogenous inducers of inflammation rather than from microbial infections.
authors.affiliation: Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de la Méditerranée, Campus de Luminy, Marseille, France.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Anfossi
authors.forename: Scott H
authors.initials: SH
authors.lastname: Robbins
authors.forename: Sophie
authors.initials: S
authors.lastname: Ugolini
authors.forename: Philippe
authors.initials: P
authors.lastname: Georgel
authors.forename: Kasper
authors.initials: K
authors.lastname: Hoebe
authors.forename: Cécile
authors.initials: C
authors.lastname: Bouneaud
authors.forename: Catherine
authors.initials: C
authors.lastname: Ronet
authors.forename: Arthur
authors.initials: A
authors.lastname: Kaser
authors.forename: Catherine B
authors.initials: CB
authors.lastname: DiCioccio
authors.forename: Elena
authors.initials: E
authors.lastname: Tomasello
authors.forename: Richard S
authors.initials: RS
authors.lastname: Blumberg
authors.forename: Bruce
authors.initials: B
authors.lastname: Beutler
authors.forename: Steven L
authors.initials: SL
authors.lastname: Reiner
authors.forename: Lena
authors.initials: L
authors.lastname: Alexopoulou
authors.forename: Olivier
authors.initials: O
authors.lastname: Lantz
authors.forename: David H
authors.initials: DH
authors.lastname: Raulet
authors.forename: Laurent
authors.initials: L
authors.lastname: Brossay
authors.forename: Eric
authors.initials: E
authors.lastname: Vivier
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000096:biosynthesis* / Q000502:physiology; D024201:Bystander Effect / Q000276:immunology; D002454:Cell Differentiation / Q000276:immunology; D002999:Clone Cells; D003602:Cytotoxicity, Immunologic; D018984:Epitopes, T-Lymphocyte / Q000096:biosynthesis* / Q000502:physiology; D005260:Female; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D037181:Lectins, C-Type; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D011948:Receptors, Antigen, T-Cell / Q000502:physiology; D055630:Receptors, NK Cell Lectin-Like; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism
chemical_list: D000950:Antigens, Ly; D018984:Epitopes, T-Lymphocyte; D015395:Histocompatibility Antigens Class I; D037181:Lectins, C-Type; D011948:Receptors, Antigen, T-Cell; D055630:Receptors, NK Cell Lectin-Like