The changes in expression of Ki-67, and CD31 in psoriatic lesions before and after etanercept treatment Ki-67 CD31

Background: Although the effectiveness of etanercept in the treatment of psoriasis is very well- established, the mechanism of action is poorly understood. It was suggested that the therapeutic effect of etanercept in psoriasis could be mediated by the inhibition of TNF expression. Although clinical trials have sometimes demonstrated a dramatic response to TNFα inhibition, only a few studies have examined the changes occuring in the skin upon TNFα inhibition. Objectives: The aim of our study was to investigate the different effects of etanercept on cell proliferation, inflammatory infiltrate, and angiogenesis in psoriasis, and to clarify the mechanism by which etanercept exerts its therapeutic effects. Methods: Methods: Methods: Methods: Methods: Clinical response, the morpho-phenotypic changes, epidermal thickness, mitotic count were analysed and the expression of CD31, proliferative marker as Ki-67, were evaluated by immunohistochemical techniques in lesional psoriatic epidermis, before and after treatment with etanercept in 11 patients. Results: In post-treatment biopsies, a decrease in the degree of epidermal hyperplasia and a significant reduction in the severity of the inflammmatory infiltrate (p<0.05) were observed. In addition, CD31 expression was significantly decreased in the dermal cellular infiltrate, (p<0.05). Ki67 expression was significantly suppressed concurrently in about 90% of cases (p<0.01). Conclusions: We suggest that etanercept may have an inhibitory effect on an initial integral component of the pathways that leads to psoriasis. Immunopharmacologic intervention in inflammatory event has the potential to improve psoriasis. Inhibition of neovascularisation may be another mechanism of action of etanercept.