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Blood, 1 September 2002, Vol. 100, No. 5, pp. 1728-1733
IMMUNOBIOLOGY
IFN- -mediated inhibition of tumor angiogenesis by natural
killer T-cell ligand,  -galactosylceramide
Yoshihiro Hayakawa,
Kazuyoshi Takeda,
Hideo Yagita,
Mark J. Smyth,
Luc Van Kaer,
Ko Okumura, and
Ikuo Saiki
From the Department of Pathogenic Biochemistry,
Institute of Natural Medicine, Toyama Medical and Pharmaceutical
University, Toyama, Japan; the Department of Immunology, Juntendo
University School of Medicine, Bunkyo-ku, Tokyo, Japan; the Cancer
Immunology Program, Sir Donald and Lady Trescowthick Laboratories,
Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia;
and the Howard Hughes Medical Institute, Department of Microbiology and
Immunology, Vanderbilt University School of Medicine, Nashville, TN.
Alpha-galactosylceramide ( -GalCer), which is a specific ligand
for CD1d-restricted variable-14 chain (V 14)
natural killer T (NKT) cells, exerts a potent antitumor effect.
We recently demonstrated that interferon- (IFN-) secreted
by both NKT cells and NK cells plays a critical role in mediating the
antimetastatic effect of -GalCer; however, the IFN--dependent
antitumor mechanisms remain poorly defined. In the present study, we
demonstrate IFN--dependent inhibition of tumor angiogenesis by
-GalCer. In -GalCer-treated mice, subcutaneous tumor growth and
tumor-induced angiogenesis were inhibited in an
IFN--dependent manner. The
-GalCer-activated splenic or hepatic mononuclear cells
inhibited murine endothelial cell proliferation in vitro, and this
inhibitory effect was mediated mostly by IFN- produced by NKT cells
and NK cells. NK cell depletion resulted in significant but partial
inhibition of tumor growth and angiogenesis in vivo. These results
suggest that the IFN--mediated inhibition of tumor angiogenesis is
critically involved in the effector mechanisms of antitumor effects
evoked by -GalCer.
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