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CUTTING EDGE |
*
Department of Internal Medicine 1, Kurume University, Kurume, Japan;
Research and Development Division, R&D Laboratories, Nippon Organon K.K., Osaka, Japan;
Institute of Molecular Embryology Genetics, Kumamoto University, Kumamoto, Japan;
Department of Nutrition and Physiological Chemistry, Osaka University Medical School, Osaka, Japan; and
¶ Laboratory of Experimental Immunology, National Cancer Institute-Frederick, Frederick, MD 21702
IL-18 has been shown to be a strong cofactor for Th1 T cell
development. However, we previously demonstrated that when IL-18 was
combined with IL-2, there was a synergistic induction of a Th2
cytokine, IL-13, in both T and NK cells. More recently, we and other
groups have reported that IL-18 can potentially induce IgE, IgG1, and
Th2 cytokine production in murine experimental models. Here, we report
on the generation of IL-18-transgenic (Tg) mice in which mature mouse
IL-18 cDNA was expressed. CD8+CD44high T cells
and macrophages were increased, but B cells were decreased in these
mice while serum IgE, IgG1, IL-4, and IFN-
levels were significantly
increased. Splenic T cells in IL-18 Tg mice produced higher levels of
IFN-, IL-4, IL-5, and IL-13 than control wild-type mice. Thus,
aberrant expression of IL-18 in vivo results in the increased
production of both Th1 and Th2 cytokines.
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