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Cutting edge: IL-18-transgenic mice: In vivo evidence of a broad role for IL-18 in modulating immune function

  1. Author:
    Hoshino, T.
    Kawase, Y.
    Okamoto, M.
    Yokota, K.
    Yoshino, K.
    Yamamura, K.
    Miyazaki, J.
    Young, H. A.
    Oizumi, K.

  2. Author Address

    Kurume Univ, Sch Med, Dept Internal Med 1, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan. Kurume Univ, Sch Med, Dept Internal Med 1, Kurume, Fukuoka 8300011, Japan. Nippon Organon KK, R&D Labs, Res & Dev Div, Osaka, Japan. Kumamoto Univ, Inst Mol Embryol Genet, Kumamoto, Japan. Osaka Univ, Sch Med, Dept Nutr & Physiol Chem, Osaka, Japan. Natl Canc Inst, Expt Immunol Lab, Frederick, MD 21702 USA. Hoshino T Kurume Univ, Sch Med, Dept Internal Med 1, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan.
    1. Year: 2001
  2. Journal: Journal of Immunology
    1. 166
    2. 12
    3. Pages: 7014-7018
  4. Type of Article: Article
  1. Abstract:

    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(+)CD44(high) T cells and macrophages were increased, but B cells were decreased in these mice while serum IgE, IgG1, IL-4, and IFN-gamma levels were significantly increased. Splenic T cells in IL-18 Tg mice produced higher levels of IFN-gamma, IL-4, IL-5, and IL-13 than control wildtype mice. Thus, aberrant expression of IL-18 in vivo results in the increased production of both Th1 and Th2 cytokines.

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