IL-1α, IL-6 and TNF-α in Cutaneous Lesions of Lupus Erythematosus are Inhibited by Topical Application of Calcipotriol

Abstract

Lupus Erythematosus (LE) is an autoimmune disorder with an unknown etiology and pathogenesis. Skin lesions of LE express several cytokines which correlate to histological findings such as IL-1 and IL-6 which are mediators of epidermal growth and proliferation. Skin lesions of LE are generally treated with immunosuppressive agents such as oral or topically applied corticosteroids. Recently a new drug, calcipotriol, a vitamin D3 analogue has been useful in treatment of psoriasis with no ad verse effect on calcium metabolism. This drug shares immunomodulatory effects with vit. D3 by inhibiting several cytokines produced by keratinocytes. In order to test the clinical effectiveness of calcipotriol in cutaneous lesions of LE we have investigated several proinflammatory cytokines such as: IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-8, MCP-1, TNF-α. Using an avidin-biotin immunoperoxidase system we have found IL-1 in both forms, IL-6 and TNF-α in basal keratinocytes in patients affected with LE, after treatment they were reverted to normal. This inhibition is induced at a molecular level as demostrated by reduced IL-1, IL-6 and TNFα mRNA expression. This is the first report showing that calcipotriol is effective in cutaneous lesions of LE and suggesting that this action is due to an inhibition of protein synthesis and mRNA expression for IL-1α, IL-6 and TNFα.