Involvement of tumor necrosis factor-related apoptosis-inducing ligand in NK cell-mediated and IFN-γ-dependent suppression of subcutaneous tumor growth

被引：116

作者：

Takeda, K

Smyth, MJ

Cretney, E

Hayakawa, Y

Yamaguchi, N

Yagita, H

Okumura, K

机构：

[1] Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

[2] Peter MacCallum Canc Inst, Sir Donald & Lady Trescowthick Labs, Canc Immunol Program, Melbourne, Vic 3002, Australia

[3] Toyama Med & Pharmaceut Univ, Res Inst Nat Med, Dept Pathogan Biochem, Toyama 9300194, Japan

[4] Juntendo Univ, Sch Med, Allergy Res Ctr, Bunkyo Ku, Tokyo 1138421, Japan

来源：

CELLULAR IMMUNOLOGY | 2001年 / 214卷 / 02期

基金：

英国医学研究理事会;

关键词：

TRAIL; NK cells; IFN-gamma; tumor growth;

D O I：

10.1006/cimm.2001.1896

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Natural killer (NK) cells and interferon- (IFN) gamma have been implicated in immune surveillance against tumor development. Here we show tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is a type II membrane protein belonging to the TNF family and plays a critical role in the NK cell-mediated and IFN-gamma-dependent suppression of subcutaneous growth of TRAIL-sensitive tumors. Administration of a neutralizing monoclonal antibody against TRAIL promoted outgrowth of subcutaneously inoculated TRAIL-sensitive tumors (L929, LB27.4, and Renca) but not TRAIL-resistant tumors (P815 and 1316). Such a protective effect of TRAIL against TRAIL-sensitive tumors was abrogated in NK cell-depleted or IFN-gamma-deficient mice. These results suggested a substantial role of TRAIL as the effector molecule that eliminates subcutaneously developing TRAIL-sensitive tumors. (C) 2001 Elsevier Science (USA).

引用

页码：194 / 200

页数：7

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