MOLECULAR MECHANISMS AND CLINICAL APPLICATION OF ULTRAVIOLET A THERAPY

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The purpose of this study was to investigate the underlying mechanisms and the clinical application of UVA1 phototherapy for skin diseases, e.g., atopic dermatitis, cutaneous T cell lymphoma and systemic sclerosis. UVA1 can penetrate through the epidermis to the deep dermis. No apoptosis was induced in keratinocytes and fibroblasts with 30-50 J/cmィイD12ィエD1 of UVA1 (430-400), which easily mediated T cell apoptosis. UVA1 induced FASL surface expression in keratinocytes if they were treated with metalloprotease inhibitor. Soluble FASL (sFASL) was also detected in the supernatant of UVA1-irradiated keratinocytes. The supernatant mediated apoptosis of FAS-expressing T cells with the treatment of the supernatant, which was partially inhibited with FASL antibody. The result suggested that sFASL from UVA1-irradiated keratinocytes mediated apoptosis of the infiltrating T cells in the lesion through paracrine mechanism. In fibroblasts, UVA1 upregulated metalloprotease (MMP)1, 3 but not TIMP-1, 3. It suggested that UVA1 might be effective for fibrous diseases, e.g., scleroderma. Based on the in vitro results, UVA1 therapy was attempted for the treatment of cutaneous malignant T cells and systemic sclerosis. The therapeutic effectiveness was found in both diseases.