Previous studies have demonstrated that herpes simplex virus-1 (HSV-1)-infected mononuclear cells are able to stimulate autologous peripheral blood mononuclear cells (PBMC) of immune donors and to activate HSV-specific cytotoxic T lymphocytes (CTL) expressing either γδ or αβ T-cell receptors (TCR). In the present report characterization of 10 γδ+ and six αβ+ HSV-specific cytotoxic T-cell colonies (TCC) is described. Cytotoxic colonies were derived from HSV-induced cell lines of three donors who, in previous experiments, had shown a prevalence of γδ+ or αβ+ effector cells. HSV-1 induced cell lines obtained from γδ+ responders included more than 80% of cells expressing Vγ9/δ2 TCR V region chains. γδ+ TCC also expressed Vγ9/δ2 molecules. αβ+ TCC all expressed CD8 antigen, while only one of 10 γδ+ TCC was CD8+, the others being CD4/CD8-double negative. The cytotoxic response of HSV-specific TCC was HLA-unrestricted; nevertheless CD8+ TCC were dependent on the expression of HLA class I on the surface of target cells to mediate cytolytic activity, while CD8- TCC were not. Blocking experiments with monoclonal antibody (mAb) specific for lymphocyte function-associated antigen-1 (LFA-1), which is expressed on all TCC, demonstrated that all αβ+ TCC and some γδ TCC also needed the interaction between LFA-1 and its ligands to develop cytotoxic activity. Altogether our data suggest that HSV-specific CTL may represent a population selected by a high concentration of antigen with a broad range of TCR affinities, which may play an important role as a first line off defence against HSV infection.

Herpes simplex virus-specific human cytotoxic T-cell colonies expressing either γδ or αβ T-cell receptor: Role of accessory molecules on HLA-unrestricted killing of virus-infected targets / Maccario, R.; Comoli, P.; Percivalle, E.; Montagna, D.; Locatelli, F.; Gerna, G.. - In: IMMUNOLOGY. - ISSN 0019-2805. - 85:1(1995), pp. 49-56.

Herpes simplex virus-specific human cytotoxic T-cell colonies expressing either γδ or αβ T-cell receptor: Role of accessory molecules on HLA-unrestricted killing of virus-infected targets

Locatelli F.;
1995

Abstract

Previous studies have demonstrated that herpes simplex virus-1 (HSV-1)-infected mononuclear cells are able to stimulate autologous peripheral blood mononuclear cells (PBMC) of immune donors and to activate HSV-specific cytotoxic T lymphocytes (CTL) expressing either γδ or αβ T-cell receptors (TCR). In the present report characterization of 10 γδ+ and six αβ+ HSV-specific cytotoxic T-cell colonies (TCC) is described. Cytotoxic colonies were derived from HSV-induced cell lines of three donors who, in previous experiments, had shown a prevalence of γδ+ or αβ+ effector cells. HSV-1 induced cell lines obtained from γδ+ responders included more than 80% of cells expressing Vγ9/δ2 TCR V region chains. γδ+ TCC also expressed Vγ9/δ2 molecules. αβ+ TCC all expressed CD8 antigen, while only one of 10 γδ+ TCC was CD8+, the others being CD4/CD8-double negative. The cytotoxic response of HSV-specific TCC was HLA-unrestricted; nevertheless CD8+ TCC were dependent on the expression of HLA class I on the surface of target cells to mediate cytolytic activity, while CD8- TCC were not. Blocking experiments with monoclonal antibody (mAb) specific for lymphocyte function-associated antigen-1 (LFA-1), which is expressed on all TCC, demonstrated that all αβ+ TCC and some γδ TCC also needed the interaction between LFA-1 and its ligands to develop cytotoxic activity. Altogether our data suggest that HSV-specific CTL may represent a population selected by a high concentration of antigen with a broad range of TCR affinities, which may play an important role as a first line off defence against HSV infection.
1995
...
01 Pubblicazione su rivista::01a Articolo in rivista
Herpes simplex virus-specific human cytotoxic T-cell colonies expressing either γδ or αβ T-cell receptor: Role of accessory molecules on HLA-unrestricted killing of virus-infected targets / Maccario, R.; Comoli, P.; Percivalle, E.; Montagna, D.; Locatelli, F.; Gerna, G.. - In: IMMUNOLOGY. - ISSN 0019-2805. - 85:1(1995), pp. 49-56.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1491222
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