RT Journal Article
SR Electronic
T1 Increased Susceptibility to Tumor Initiation and Metastasis in TNF-Related Apoptosis-Inducing Ligand-Deficient Mice
JF The Journal of Immunology
JO J. Immunol.
FD American Association of Immunologists
SP 1356
OP 1361
DO 10.4049/jimmunol.168.3.1356
VO 168
IS 3
A1 Cretney, Erika
A1 Takeda, Kazuyoshi
A1 Yagita, Hideo
A1 Glaccum, Moira
A1 Peschon, Jacques J.
A1 Smyth, Mark J.
YR 2002
UL http://www.jimmunol.org/content/168/3/1356.abstract
AB 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 α-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.