| Seq #289 | Saturday, 13 March 2004 | |||||||
| 7:00 AM-7:45 AM Hawaii Convention Center Ballroom, Plenary | ||||||||
| Molecular Mechanisms of Cell-mediated Killing and Tumor Rejection | ||||||||
Sponsored by: Plenary | ||||||||
| Description: Cytotoxic T-lymphocytes (CTL), natural killer (NK) cells, and recently found natural killer T (NKT) cells play important roles in immunosurveillance against tumor cells and virus-infected cells. Here, we report the biological relevance of molecules involved in cell-mediated killing, such as perforin and tumor necrosis factor (TNF) families, to tumor rejection. Although perforin, the main cytotoxic molecule of CTL, NK cells, and NKT cells, appears to be the critical molecule for tumor rejection in some experimental models as previously reported, TNF-related apoptosis-inducing ligand (TRAIL) is the vital component of immunosurveillance of spontaneous or resident tumor cells by both T-cells and NK cells. Administration of the agonistic antibody against apoptosis-inducible TRAIL receptor (DR5) inhibited tumor metastasis and growth of TRAIL-sensitive tumors, which resulted in CTL induction and perforin- and FasL-dependent secondary tumor rejection. Our findings will stimulate more hope that manipulating TRAIL activity is an effective path to improved cancer immunotherapy | ||||||||
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Back to the IADR/AADR/CADR 82nd General Session (March 10-13, 2004)