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In vivo effects of cytokines on psoriatic skin grafted on nude mice: involvement of the tumour necrosis factor (TNF) receptor

Following engraftment of human involved psoriatic skin to nude mice there is a partial normalization of pathology associated with a loss of inflammatory leucocytes. However, the epidermis remains hyperproliferative, which may reflect a primary defect. The roles of TNF‐α, IL‐1 and IL‐6 in epidermal hyperproliferation of grafted psoriatic lesions were investigated. Before and after treatment, grafts were analysed to determine epidermal thickness and labelling index (LI). HLA‐DR, intercellular adhesion molecule‐1 (ICAM‐1), and TNF receptor (TNF‐R; p75 and p55) expression were determined by immunoperoxidase staining. Psoriatic epidermis was found consistently to be negative for p55 TNF‐R and p75 TNF‐R before grafting. Following engraftment, TNF‐R‐positive cells (i.e. p55 by keratinocytes; p75 by epidermal dendritic cells) were identified throughout the epidermis. Higher numbers of p75 TNF‐R epidermal dendritic cells were found in grafts following a course of TNF‐α, IL‐6 or IL‐1 treatment. The p55 form of the TNF‐R expressed by keratinocytes was significantly elevated after treatment with TNF‐α or IL‐6. HLA‐DR and ICAM‐1 were also expressed in these grafts. TNF‐α, anti‐IL‐1, and anti‐IL‐6 treatment induced a marked decrease in the epidermal thickness and LI of psoriatic graft tissue, correcting the hyperproliferation associated with psoriatic epidermis. Supraphysiological levels of TNF‐α may saturate and consequently down‐regulate their own receptors, leading to a paradoxical inhibitory effect.