Background: IL-18 was originally cloned as a IFN-${gamma}$ inducing factor in primed T cells. In synergy with IL-12, IL-18 has been shown to induce strikingly high levels of IFN-${gamma}$ production by T cells and to enhance Th1 development. Also this cytokine exerts induction of Th2 development through IL-4 induction. Methods: Resting $CD4^+$ T cells were sorted by negative selection and activated by anti-CD3 plus anti-CD28 Ab. Expression of IL-12 binding sites, IL-18 binding sites, IL-18R ${alpha}$, and GATA-3 mRNA were analysed by FACS and RT-PCR, respectively. Results: Resting $CD4^+$ T cells expressed IL-18R ${alpha}$ chain but not IL-18 binding sites, suggesting a lack of IL-18R ${eta}$ expression. IL-18R ${alpha}$ was maintained on the Th1 and Th2 committed cells. IL-18 binding sites were induced on the Th1 but not Th2 cells. Exposure of these cells to IL-18 led to up-regulation of GATA-3 mRNA expression only in Th2 committed cells. To elucidate the relationship between IL-18R ${alpha}$ expression and GATA-3 induction by IL-18, Th1 and Th2 committed cells were further cultured in medium with or without IL-12 for 2 days. IL-12 binding sites were maintained on the Th1 and Th2 cells regardless of IL-12 treatment, but IL-18R a expression was rapidly down-regulated on the IL12-untreated Th2 cells which did not induce GATA-3 mRNA expression followed by IL-18 stimulation. Conclusion: IL-12 supports expression of IL-18R ${alpha}$ and GATA-3 mRNA expression was induced by IL-18 through IL-18R ${alpha}$ without expression of IL-18 binding site in Th2 cells.