Interleukin-18 was first described as an interferon-γ (IFN-γ) inducing factor. In general, IL-18 induction of IFN-γ is similar to that of IL-12, when it is a sole cytokine. IL-18 induces low levels of IFNγ, but in the presence of co-stimulants, IFN-γ production is greatly enhanced [6] . However, because antibodies to IL-18 also reduced the hepatotoxicity of endotoxaemia, IL-18 was considered to possess other biological properties beyond that of inducing IFN-γ [7] . IL-18 activates T cells to synthesize IL-2, GM-CSF, and TNF-α. There are also reports that IL-18 suppresses the production of IL-10 and does not induce the production of IL-1Ra. In general, the ability of IL-18 to induce different cytokines depends on the cellular targets [8] . Flisiak et al. confirmed an association between plasma IL-18 concentration and psoriasis severity. Moreover, it was shown that combined measurement of IL-18 and TGF-beta1 in plasma can be considered as a possible biomarker of psoriasis activity [9] . Kato et al. indicated that a single nucleotide polymorphism (SNP) in the promoter of the interleukin-18 gene is associated with the presence of psoriasis, but not atopic dermatitis. This suggests that the SNP is associated with susceptibility to psoriasis vulgaris, presumably by affecting the production of IL-18 [10] .