title: Liver CD4-CD8- NK1.1+ TCR alpha beta intermediate cells increase during experimental malaria infection and are able to exhibit inhibitory activity against the parasite liver stage in vitro.
abstract: Experimental infection of C57BL/6 mice by Plasmodium yoelii sporozoites induced an increase of CD4-CD8- NK1.1+ TCR alpha beta int cells and a down-regulation of CD4+ NK1.1+ TCR alpha beta int cells in the liver during the acute phase of the infection. These cells showed an activated CD69+, CD122+, CD44high, and CD62Lhigh surface phenotype. Analysis of the expressed TCRV beta segment repertoire revealed that most of the expanded CD4-CD8- (double-negative) T cells presented a skewed TCRV beta repertoire and preferentially used V beta 2 and V beta 7 rather than V beta 8. To get an insight into the function of expanded NK1.1+ T cells, experiments were designed in vitro to study their activity against P. yoelii liver stage development. P. yoelii-primed CD3+ NK1.1+ intrahepatic lymphocytes inhibited parasite growth within the hepatocyte. The antiplasmodial effector function of the parasite-induced NK1.1+ liver T cells was almost totally reversed with an anti-CD3 Ab. Moreover, IFN-gamma was in part involved in this antiparasite activity. These results suggest that up-regulation of CD4-CD8- NK1.1+ alpha beta T cells and down-regulation of CD4+ NK1.1+ TCR alpha beta int cells may contribute to the early immune response induced by the Plasmodium during the prime infection.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale U313, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires, CHU Pitié-Salpêtrière, Paris, France. spied@pasteur.fr
authors.forename: S
authors.initials: S
authors.lastname: Pied
authors.forename: J
authors.initials: J
authors.lastname: Roland
authors.forename: A
authors.initials: A
authors.lastname: Louise
authors.forename: D
authors.initials: D
authors.lastname: Voegtle
authors.forename: V
authors.initials: V
authors.lastname: Soulard
authors.forename: D
authors.initials: D
authors.lastname: Mazier
authors.forename: P A
authors.initials: PA
authors.lastname: Cazenave
mesh_terms: D000818:Animals; D000941:Antigens / Q000096:biosynthesis; D000950:Antigens, Ly; D000954:Antigens, Surface; D015704:CD4 Antigens / Q000096:biosynthesis; D016827:CD8 Antigens / Q000096:biosynthesis; D002478:Cells, Cultured; D015536:Down-Regulation / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D019674:Genes, T-Cell Receptor beta; D037181:Lectins, C-Type; D008099:Liver / Q000276:immunology / Q000469:parasitology* / Q000473:pathology; D008109:Liver Diseases, Parasitic / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology; D018655:Lymphocyte Count; D008288:Malaria / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology*; D051379:Mice; D008810:Mice, Inbred C57BL; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010967:Plasmodium yoelii / Q000254:growth & development* / Q000276:immunology*; D014176:Protein Biosynthesis; D011506:Proteins; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000096:biosynthesis / Q000235:genetics; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology
chemical_list: D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D015704:CD4 Antigens; D016827:CD8 Antigens; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D016693:Receptors, Antigen, T-Cell, alpha-beta