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The Journal of Immunology, 1998, 161: 3400-3407.
Copyright © 1998 by The American Association of Immunologists

IL-12 Up-Regulates IL-18 Receptor Expression on T Cells, Th1 Cells, and B Cells: Synergism with IL-18 for IFN-{gamma} Production1

Tomohiro Yoshimoto*,{dagger}, Kiyoshi Takeda{ddagger}, Takashi Tanaka{ddagger}, Kazunobu Ohkusu*, Shin-ichiro Kashiwamura{dagger}, Haruki Okamura{dagger}, Shizuo Akira{ddagger} and Kenji Nakanishi2,*,{dagger}

* Department of Immunology and Medical Zoology, {dagger} Laboratory of Host Defenses, Institute for Advanced Medical Sciences, and {ddagger} Department of Biochemistry, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan

IL-18 is a product of macrophages and with IL-12 strikingly induces IFN-{gamma} production from T, B, and NK cells. Furthermore, IL-18 and IL-12 synergize for IFN-{gamma} production from Th1 cells, although this combination fails to affect Th2 cells. In this study, we show that IL-12 and IL-18 promptly and synergistically induce T and B cells to develop into IFN-{gamma}-producing cells without engaging their Ag receptors. We also studied the mechanism underlying differences in IL-18 responsiveness between Th1 and Th2 cells. Pretreatment of T or B cells with IL-12 rendered them responsive to IL-18, which induces cell proliferation and IFN-{gamma} production. These IL-12-stimulated cells had both high and low affinity IL-18R and an increased IL-18R mRNA expression. In particular, IL-12-stimulated T cells strongly and continuously expressed IL-18R mRNA. However, when T cells developed into Th1 cells after stimulation with anti-CD3 and IL-12, they lowered this IL-12-induced-IL-18R mRNA expression. Then, such T cells showed a dominant response to anti-CD3 by IFN-{gamma} production when they were subsequently stimulated with anti-CD3 and IL-18. In contrast, Th2 cells did not express IL-18R mRNA and failed to produce IFN-{gamma} in response to anti-CD3 and IL-18, although they produced a substantial amount of IFN-{gamma} in response to anti-CD3 and IL-12. However, when Th1 and Th2 cells were stimulated with anti-CD3, IL-12, and IL-18, only the Th1 cells markedly augmented IFN-{gamma} production in response to IL-18, suggesting that IL-18 responsiveness between Th1 and Th2 cells resulted from their differential expression of IL-18R.




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