title: Vgamma9Vdelta2 T cells use a combination of mechanisms to limit the spread of the pathogenic bacteria Brucella.
abstract: Human Vgamma9Vdelta2 T cells play a crucial role in early immune response to intracellular pathogens. In brucellosis infection, this population of cells is drastically increased in the peripheral blood of patients during the acute phase of infection. In vitro, Vgamma9Vdelta2 T cells exhibit strong cytolytic activity against Brucella-infected cells and are able to impair intracellular growth of Brucella suis in autologous macrophages. In this study, we have investigated the relative importance of contact-dependent mechanisms versus soluble factors in the intracellular growth and viability of B. suis. We show that Vgamma9Vdelta2 T cells use contact-dependent mechanisms, such as the release of lytic granules and Fas-mediated signals, to decrease intracellular B. suis through lysis of infected macrophages, but these mechanisms have little impact on Brucella survival. Moreover, we demonstrate that soluble factors secreted by Vgamma9Vdelta2 T cells can directly affect B. suis survival through their potent bactericidal effects. From these results, we conclude that Vgamma9Vdelta2 T cells are able to use a combination of mechanisms that reduce the total numbers of B. suis and thus, may benefit the host by limiting the spread of this intracellular pathogen.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale Unité 431, Microbiologie et Pathologie Cellulaire Infectieuse, Université de Montpellier II, Place Eugene Bataillon, CC 100, 34095 Montpellier Cedex 05, France.
authors.forename: Jane
authors.initials: J
authors.lastname: Oliaro
authors.forename: Sherri
authors.initials: S
authors.lastname: Dudal
authors.forename: Janny
authors.initials: J
authors.lastname: Liautard
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Andrault
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Liautard
authors.forename: Virginie
authors.initials: V
authors.lastname: Lafont
mesh_terms: D001770:Blood Bactericidal Activity / Q000276:immunology*; D041021:Brucella suis / Q000276:immunology*; D002006:Brucellosis / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology*; D002470:Cell Survival / Q000276:immunology; D002478:Cells, Cultured; D005089:Exocytosis / Q000276:immunology; D053222:Fas Ligand Protein; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000382:microbiology; D008562:Membrane Glycoproteins / Q000276:immunology; D009000:Monocytes / Q000276:immunology* / Q000382:microbiology; D016692:Receptors, Antigen, T-Cell, gamma-delta; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D019014:fas Receptor / Q000276:immunology
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D016692:Receptors, Antigen, T-Cell, gamma-delta; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D007371:Interferon-gamma