| Summary: | 碩士 === 國立海洋大學 === 生物科技研究所 === 91 === The role of Fas ligand (FasL) in programmed cell death via interaction with its receptor Fas is well characterized. It has been proposed that expression of FasL can confer immune privilege to some organs, allowing them to kill infiltrating lymphocytes and inflammatory cells. However, a number of studies have shown that when tumors or transplants express FasL, rejection often occurs as a consequence of proinflammatory functions of FasL. Here we demonstrate that FasL elicits tumor immunity in murine lung carcinoma (LLC-1) and transitional cell carcinoma (MBT2) models. C57BL/6 mice were injected sc with LLC-FasL cells, and 100% remained tumor-free. When these tumor-free vaccinated mice were challenged with LLC-1 (WT), the re-challenged tumors were able to be rejected in the 60% mice. To compare with control, CTL response is up to 32.78% specific lysis. In transitional cell carcinoma model, we could not obtain FasL-expressing MBT2 cell line. Using transient transfection, FasL-expressing MBT2 could reduce tumor growth. These results suggest that FasL a potential therapeutic approach may be used for cancer gene therapy.
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