Induction of anti-hepatoma immunity by recombinant retrovirus expressing B7-1 /B7-2 costimulatory mo

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Objective: To construct recombinant R7-l/B7-2 retrovirus vectors and observe the effects of B7-l/R7-2 gene expression on in ho and in for immune response against against murine hepatoma. Methods: The recombinant retrovirus vectors expressing B7-1/B7-2 were constructed by gene cloning technology to produce retrovirus-infected PE501 and PA317 cell lines and murine hepatoma Hepal-6. The expression of R7-l/B7-2 was detected by fluorescence activated cell soning analysis (FACS). B7-l/B7-2 positive Hepal-6 Cell lines were used in inducing anti-hepatoma immunity in ho and in the. Results: In contrast to the excessive growth of parental Hemal-6 tumor, the growth of B7-l/B7-2-positive Hepal-6 inoculated into syngenic mice regressed. B7-1/R7-2-positive or cytokine-treated Hepal-6 alone could only induce mild cytototicity; in contrast, B7-1/B7-2-positive Hemal-6 treated with cytokine-stimulated spleen cells and activated the cytotoxicity effectively. Immunity in mice with R7-1/B7-2-positive tumor cells or cytokine-beated Hepal-6 only provided partial protection against parental Hepa1-6 tumor, whereas pretreatment of the transfected tumor cells with IFN-r and TNF-a induced complete immunity protection in vivo. Mice receiving inoculation of cytokine-treated B7-l/R7-2-positive Hemal-6 cells presented regression of the establoshed pental tUmor and survived for more than l00 d, while those untreated mice died within 40 d. Conclu sions: B7-l/R7-2 expression is necessary but not sufficient in inducing anti-hepatoma immune response, whereas it is efficient when combined with the beatment of IFN-γ and TNF-a. Objective: To construct recombinant R7-1 / B7-2 retrovirus vectors and observe the effects of B7-1 / R7-2 gene expression on in ho and in for immune response against murine hepatoma. Methods: The recombinant retrovirus vectors expressing B7- 1 / B7-2 were constructed by gene cloning technology to produce retrovirus-infected PE501 and PA317 cell lines and murine hepatoma Hepal-6. The expression of R7-1 / B7-2 was detected by fluorescence activated cell soning analysis (FACS). B7-1 / B7-2 positive Hepal-6 Cell lines were used in inducing anti-hepatoma immunity in ho and in the. Results: In contrast to the excessive growth of parental Hemal-6 tumor, the growth of B7-1 / B7 -2-positive Hepal-6 inoculated into syngenic mice regressed. B7-1 / R7-2-positive or cytokine-treated Hepal-6 alone could only induce mild cytototicity; in contrast, B7-1 / B7-2- 6 treated with cytokine-stimulated spleen cells and activated the cytotoxicity effectively. Immunity in mice with R7-1 / B7-2-positive tum or cells or cytokine-beated Hepal-6 only partial protection against parental Hepa 1-6 tumors, and pretreatment of the transfected tumor cells with IFN-r and TNF-a induced complete immunity protection in vivo. Mice receiving inoculation of cytokine-treated B7 -l / R7-2-positive Hemal-6 cells presented regression of the established pental tUmor and survived for more than l00d, while those untreated mice died within 40d. Conclu sions: B7-1 / R7-2 expression is necessary but not sufficient in inducing anti-hepatoma immune response, but it is efficient when combined with the beat of of IFN-γ and TNF-a.
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