Abstract
We hypothesized that inducing display of the IgFc molecule on the tumor cell surface by gene transfer would promote tumor cell killing by the same mechanisms as antibody based approaches, but would alleviate some of the problems inherent in the use of antibodies for cancer therapy. We expressed the cDNA of the Fc portion of the murine IgG2a heavy chain on the surface of tumor cells thereby mimicking a natural antibody tagging event. In vitro, Fc receptor positive natural killer cells specifically recognized and lysed B16 melanoma cells expressing surface IgFc. Macrophages bound to B16-Fc, cells significantly more than to parental B16 and surface IgFc expression promoted formation of the terminal complement pore complex. Expression of the IgFc dramatically delayed the ability of B16 cells to form tumors in vivo, dependent on macrophages and NK cells.
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