Psoriasis is a common chronic inflammatory skin disease. It frequently develops in early adulthood although all ages can be affected. Once psoriasis appears, it is usually a life-long disease without spontaneous improvement. The skin lesion of the disease is characterized by erythematous scaly patches or plaques, caused by hyperproliferation and abnormal or incomplete differentiation of epidermal keratinocyte, together with chronic inflammatory cell infiltrate in both the dermis and epidermis1. In its pathogenesis, psoriasis is considered as T-cell mediated inflammatory disease and various inflam­matory cytokines such as tumor necrotic factor (TNF)-a and interferon (IFN)-y are likely to play major functions. Although inflammatory cells seem to play a central role, it is probably best to conceptualize the pathogenesis as an interactive response between genetics, inflammatory cells, resident skin cells and an array of immunologic cascades between these. A strong association has been well established between chronic inflammatory conditions and carcinogenesis, and although psoriasis also has many characteristics prone to malignant transformation, conversion of a psoriatic lesion to skin cancer is extremely rare.

Telomere is the nucleoprotein structure that caps the end of eukaryotic chromosomes, which main­tains chromosomal stability. It contributes not only to senescence, but also to the provision of an effective tumor suppressor mechanism. Among somatic cells, telomerase activity is demonstrated in the keratinocyte of the proliferatory basal layer of the epidermis. There is also evidence of increased telomerase activity in nonmalignant skin conditions such as psoriasis vulgaris.

In this study, we demonstrated that TNF-a and INF-y, key cytokines in psoriasis development, increased telomerase activity on the cultured human keratinocyte. levitra plus

Moreover, the effect of TNF-a and INF-y were more prominent at the early passage of cultures, which contain more proliferatory cells. It might be suggested that these cytokines increase telomerase activity especially on the proliferatory cells, which might lead to abnormal keratinization of psoriatic skin lesions. In addition, these results could partially explain the reason for the rare incidence of cancer development in psoriasis even though it fulfills many conditions for carcinogenesis.