In the present study our patients with psoriasis showed significantly increased IL-18 expression in keratinocytes from psoriatic lesions before and after receiving medication whether topical or systemic in comparison to keratinocytes from non-lesional skin. This supports the concept viewing psoriasis as a T-cell-mediated autoimmune disease. Krueger [18] reported, in his study on a large series of skin biopsies, increased protein expression in lesional as opposed to non-lesional skin samples. Other investigators stated that lesional skin might be the source of the elevated plasma levels of IL-18 [19] . In the present work quantitative PCR using mRNA taken from uninvolved skin revealed low but detectable levels of IL-18 mRNA expression. This finding is consistent with previous studies showing that human keratinocytes are capable of synthesizing low levels of IL-18 mRNA even under non-stimulated conditions [20] . Chang et al. [21] found that genes specifically modulated in uninvolved skin play a major role in triggering disease progression, and in being the first candidate for early disease diagnosis or development of new therapies. This finding could allow selection of the treatment regimen for individual patients.