Increased Susceptibility to Tumor Initiation and Metastasis in TNF-Related Apoptosis-Inducing Ligand-Deficient Mice | Zendy

Erika Cretney | Zendy; Kazuyoshi Takeda | Zendy; Hideo Yagita∥ | Zendy; Moira Glaccum | Zendy; Jacques J. Peschon | Zendy; Mark J. Smyth | Zendy

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Increased Susceptibility to Tumor Initiation and Metastasis in TNF-Related Apoptosis-Inducing Ligand-Deficient Mice

Author(s) -

Erika Cretney,

Kazuyoshi Takeda,

Hideo Yagita∥,

Moira Glaccum,

Jacques J. Peschon,

Mark J. Smyth

Publication year - 2002

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.168.3.1356

Subject(s) - tumor necrosis factor alpha , effector , cancer research , gene targeting , spleen , biology , innate immune system , metastasis , apoptosis , immune system , cytotoxicity , immunology , peripheral blood mononuclear cell , gene knockout , gene , cancer , in vitro , genetics

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.

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