First Author | Cretney E | Year | 2002 |
Journal | J Immunol | Volume | 168 |
Issue | 3 | Pages | 1356-61 |
PubMed ID | 11801676 | Mgi Jnum | J:73948 |
Mgi Id | MGI:2157226 | Doi | 10.4049/jimmunol.168.3.1356 |
Citation | Cretney E, et al. (2002) Increased susceptibility to tumor initiation and metastasis in TNF-related apoptosis-inducing ligand-deficient mice. J Immunol 168(3):1356-61 |
abstractText | We have previously implicated TNF-related apoptosis-inducing ligand (TRAIL) in innate immune surveillance against tumor development. In this study, we describe the use of TRAIL gene-targeted mice to demonstrate the key role of TRAIL in suppressing tumor initiation and metastasis. Liver and spleen mononuclear cells from TRAIL gene-targeted mice were devoid of TRAIL expression and TRAIL-mediated cytotoxicity. TRAIL gene-targeted mice were more susceptible to experimental and spontaneous tumor metastasis, and the immunotherapeutic value of alpha-galactosylceramide was diminished in TRAIL gene-targeted mice. TRAIL gene-targeted mice were also more sensitive to the chemical carcinogen methylcholanthrene. These results substantiated TRAIL as an important natural effector molecule used in the host defense against transformed cells. |