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Shufang Liang – One of the best experts on this subject based on the ideXlab platform.

  • a novel strategy for tumour therapy combining cell apoptosis and Active Immunity induced by caspy2 a zebrafish caspase
    Journal of Cellular and Molecular Medicine, 2009
    Co-Authors: Lei Liu, Hongxin Deng, Yongsheng Wang, Ping Chen, Yang Yang, Hanshuo Yang, Xiancheng Chen, Lijuan Chen, Wen Zhu, Shufang Liang

    Abstract:

    Caspy2, a zebrafish protease, is an Active caspase for inducing apoptosis in mammalian cells. To investigate whether caspy2-mediated apoptosis could be used in cancer therapy, its cDNA was amplified and cloned into eukaryotic expression vector pcDNA3.1+. The recombinant plasmid was mixed with cationic liposome and introduced into various tumour cell lines in vitro. Our data showed that caspy2 induced remarkable apoptosis of cancer cells in vitro. Treatment of mice-bearing CT26 colon carcinoma or MethA fibrosarcoma with intratumoral injection of liposome-caspy2 plasmid complex resulted in substantial killing of neoplastic cells and long-term survivors. Apoptotic cells were widely distributed in caspy2-treated tumour tissue. Infiltration of CD8+ T lymphocyte was also observed apparently in the tumour tissue after the treatment with caspy2. Tumour-specific major histocompatibility complex (MHC) class I-dependent CD8+ cytotoxic T lymphocyte activity was found by means of 51Cr release assay. In MethA model, the mice acquired a long-time protective Immunity against the parental tumour cell re-challenge. These results indicated that caspy2 can act as both apoptosis inducer and immune response initiator, which may account for its extraordinary antitumour effect. Furthermore, in vivo depletion of CD8+ T lymphocytes could completely abrogate the antitumour immune activity, whereas the depletion of CD4+ cells showed partial abrogation. In this study, we developed a novel anticancer strategy that combines both induction of apoptosis and immune response in mice-bearing tumours with a single caspy2 gene. This approach may provide an important way for treatment of cancer.

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D C Wright – One of the best experts on this subject based on the ideXlab platform.

  • Mice are Actively immunized after passive monoclonal antibody prophylaxis and ricin toxin challenge. (Reannouncement with new availability information)
    , 1992
    Co-Authors: P V Lemley, D C Wright

    Abstract:

    Mice passively immunized by a protective, anti-ricin A-chain monoclonal antibody, then challenged intravenously with ricin, were protected from a subsequent ricin challenge, and were Actively immunized. Two significant advantages accrued from this experiment: the monoclonal antibody neutralized the toxicity of the ricin immunogen, and Active immunization was achieved with very low antigen load (approx. 0.5 micrograms/mouse). We ruled out the possibility that residual monoclonal antibody provided the protection by using three independent criteria. There was significant (four orders of magnitude) enhancement of the immune response in the presence of the monoclonal antibody; control immunizations of mice with ricin A-chain, ricin B-chain or either chain with the monoclonal antibody did not induce Active Immunity; and the Active immunization could not be replicated when protective goat polyclonal antibody was substituted for the monoclonal antibody. Because high titers were achieved rapidly without any adjuvant, we are currently investigating haptenized ricin to determine if anti-hapten monoclonal antibodies can be produced by this refined procedure.

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  • Mice are Actively immunized after passive monoclonal antibody prophylaxis and ricin toxin challenge.
    Immunology, 1992
    Co-Authors: P V Lemley, D C Wright

    Abstract:

    Mice passively immunized by a protective, anti-ricin A-chain monoclonal antibody, then challenged intravenously with ricin, were protected from a subsequent ricin challenge, and were Actively immunized. Two significant advantages accrued from this experiment: the monoclonal antibody neutralized the toxicity of the ricin immunogen, and Active immunization was achieved with very low antigen load (approximately 0.5 microgram/mouse). We ruled out the possibility that residual monoclonal antibody provided the protection by using three independent criteria. There was significant (four orders of magnitude) enhancement of the immune response in the presence of the monoclonal antibody; control immunizations of mice with ricin A-chain, ricin B-chain or either chain with the monoclonal antibody did not induce Active Immunity; and the Active immunization could not be replicated when protective goat polyclonal antibody was substituted for the monoclonal antibody. Because high titres were achieved rapidly without any adjuvant, we are currently investigating haptenized ricin to determine if anti-hapten monoclonal antibodies can be produced by this refined procedure.

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Lei Liu – One of the best experts on this subject based on the ideXlab platform.

  • a novel strategy for tumour therapy combining cell apoptosis and Active Immunity induced by caspy2 a zebrafish caspase
    Journal of Cellular and Molecular Medicine, 2009
    Co-Authors: Lei Liu, Hongxin Deng, Yongsheng Wang, Ping Chen, Yang Yang, Hanshuo Yang, Xiancheng Chen, Lijuan Chen, Wen Zhu, Shufang Liang

    Abstract:

    Caspy2, a zebrafish protease, is an Active caspase for inducing apoptosis in mammalian cells. To investigate whether caspy2-mediated apoptosis could be used in cancer therapy, its cDNA was amplified and cloned into eukaryotic expression vector pcDNA3.1+. The recombinant plasmid was mixed with cationic liposome and introduced into various tumour cell lines in vitro. Our data showed that caspy2 induced remarkable apoptosis of cancer cells in vitro. Treatment of mice-bearing CT26 colon carcinoma or MethA fibrosarcoma with intratumoral injection of liposome-caspy2 plasmid complex resulted in substantial killing of neoplastic cells and long-term survivors. Apoptotic cells were widely distributed in caspy2-treated tumour tissue. Infiltration of CD8+ T lymphocyte was also observed apparently in the tumour tissue after the treatment with caspy2. Tumour-specific major histocompatibility complex (MHC) class I-dependent CD8+ cytotoxic T lymphocyte activity was found by means of 51Cr release assay. In MethA model, the mice acquired a long-time protective Immunity against the parental tumour cell re-challenge. These results indicated that caspy2 can act as both apoptosis inducer and immune response initiator, which may account for its extraordinary antitumour effect. Furthermore, in vivo depletion of CD8+ T lymphocytes could completely abrogate the antitumour immune activity, whereas the depletion of CD4+ cells showed partial abrogation. In this study, we developed a novel anticancer strategy that combines both induction of apoptosis and immune response in mice-bearing tumours with a single caspy2 gene. This approach may provide an important way for treatment of cancer.

    Free Register to Access Article