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as an Amplifying Factor in IL-12 Induction of the Functional IL-18 Receptor Complex1
*
Department of Oncology, Biomedical Research Center, Osaka University Graduate School of Medicine, Osaka, Japan;
Department of Microbiology, Kyun-Hee University Medical School, Seoul, Korea; and
Fujisaki Institute, Hayashibara Biochemical Laboratories, Okayama, Japan
IL-12 and IL-18 are both proinflammatory cytokines that contribute
to promoting Th1 development and IFN-
expression. However, neither
IL-12R nor IL-18R is expressed as a functional complex on most resting
T cells. This study investigated the molecular mechanisms underlying
the induction of an IL-18R complex in T cells. Resting T cells
expressed IL-18R
chains but did not exhibit IL-18 binding sites as
detected by incubation with rIL-18 followed by anti-IL-18 Ab,
suggesting a lack of IL-18R
expression in resting T cells. Although
they also failed to express IL-12R, stimulation with anti-CD3 plus
anti-CD28 generated IL-12R. Exposure of these cells to IL-12 led
not only to up-regulation of IL-18R expression but also to induction
of IL-18R binding sites on both CD4+ and CD8+ T
cells concomitant with IL-18R mRNA expression. The IL-18 binding
site represented a functional IL-18R complex capable of exhibiting
IL-18 responsiveness. IL-12 induction of an IL-18R complex and
IL-18R mRNA expression was not observed in STAT4-deficient
(STAT4-/-) T cells and was substantially decreased in
IFN--/- T cells. However, the failure of
STAT4-/- T cells to induce an IL-18R complex was not
corrected by IFN-. These results indicate that STAT4 and IFN-
play an indispensable role and a role as an amplifying factor,
respectively, in IL-12 induction of the functional IL-18R
complex.
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