engleski

Expression of TNF-related cytokines TRAIL and TWEAK in psoriasis: implications in inflammation and epidermal proliferation

Psoriasis is an immune-based chronic skin disease characterized by hyperproliferation of keratinocytes and inflammatory dermal infiltrate. The clinical efficacy of tumor-necrosis factor alpha (TNF-α) -targeted therapeutics highlights the importance of this cytokine in psoriasis pathogenesis. We aimed to investigate the possible role of two relatively new members of the TNF superfamily of cytokines in psoriasis, the TNF-related apoptosis- inducing ligand (TRAIL) and TNF-like weak inducer of apoptosis (TWEAK). As evidenced by immunohistochemical and double- immunofluorescent analyses, TRAIL is abundantly present in psoriatic plaques, both in the hyperplastic epidermis and within the CD4+ and CD8+ lymphocytes, CD68+ macrophages and CD11c+ dermal dendritic cells. This cytokine probably mediates its effects through DR5 and DcR2 receptors on macrophages and endothelial cells and DcR1 on neutrophils. Conversely, expression of TWEAK is significantly decreased in psoriatic lesions, especially in lesions characterized by high rate of PCNA+ nuclei. We conclude that TRAIL significantly contributes to cytokine network in psoriasis, whereas TWEAK seems to reflect the disturbed keratinocytes’ differentiation in this disease.

Psoriasis; TRAIL; TWEAK

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