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-Galactosylceramide in Mice
*
Pharmaceutical Research Laboratory, Kirin Brewery Company, Takasaki, Japan; and
Division of Basic Traumatology, National Defense Medical College Research Institute, Tokorozawa, Japan
The role of mouse liver NK1.1 Ag+ T (NKT) cells
in the antitumor effect of 
-galactosylceramide (-GalCer) has been
unclear. We now show that, whereas -GalCer increased the serum
IFN-
concentration and alanine aminotransferase activity in NK
cell-depleted C57BL/6 (B6) mice and B6-beige/beige mice
similarly to its effects in control B6 mice, its enhancement of the
antitumor cytotoxicity of liver mononuclear cells (MNCs) was abrogated.
Depletion of both NK and NKT cells in B6 mice reduced all these effects
of -GalCer. Injection of Abs to IFN- also inhibited the
-GalCer-induced increase in antitumor cytotoxicity of MNCs.
-GalCer induced the expression of Fas ligand on NKT cells in the
liver of B6 mice. Whereas -GalCer did not increase serum alanine
aminotransferase activity in B6-lpr/lpr mice and
B6-gld/gld mice, it increased the antitumor cytotoxicity of
liver MNCs. The -GalCer-induced increase in survival rate apparent
in B6 mice injected intrasplenically with B16 tumor cells was abrogated
in beige/beige mice, NK cell-depleted B6 mice, and B6 mice
treated with Abs to IFN-. Depletion of CD8+ T cells did
not affect the -GalCer-induced antitumor cytotoxicity of liver MNCs
but reduced the effect of -GalCer on the survival of B6 mice. Thus,
IFN- produced by -GalCer-activated NKT cells increases both the
innate antitumor cytotoxicity of NK cells and the adaptive antitumor
response of CD8+ T cells, with consequent inhibition of
tumor metastasis to the liver. Moreover, NKT cells mediate
-GalCer-induced hepatocyte injury through Fas-Fas ligand
signaling.
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