UVA-INDUCED IMMUNE SUPPRESSION IN HUMAN SKIN - PROTECTIVE EFFECT OF VITAMIN-E IN HUMAN EPIDERMAL-CELLS IN-VITRO

UVA (320-400 nm) radiation damage to membranes, proteins, DNA and othe r cellular targets is predominantly related to oxidative processes. In the present study, we demonstrated that cutaneous UVA-induced immunos uppression can be related, at least in part, to the appearance of thes e oxidative processes. The UVA-induced oxidative processes in freshly isolated epidermal cells were monitored by measuring the thiobarbituri c acid reactive substances (TBARS) as an index of peroxidation. The in vitro immunosuppressive effects of UVA were demonstrated by measuring the allogeneic lymphocyte proliferation induced by epidermal cells or purified Langerhans cells in the mixed epidermal cell-lymphocyte reac tion (MECLR). In addition, the effects of a potent antioxidant (vitami n E) on these two UVA-induced processes were analysed. Our results sho wed that the antigen-presenting function of Langerhans cells measured in the MECLR is dose-dependently decreased by UVA radiation (up to 20 J/cm(2)). Overnight incubation of epidermal cells with vitamin E (400 mu mol/l) before irradiation partially protected epidermal cells from the immunosuppressive effects of UVA radiation, and decreased TBARS re lease into the supernatant (a decrease of 35% compared with a control without vitamin E). Our results suggest that UVA radiation may alter c ell-presenting antigen function partly via the generation of reactive oxygen species which trigger peroxidative processes, and these data co ntribute to the understanding of the role of oxidative mechanisms in i mmune suppression induced by UVA radiation. Our in vitro model can be used to quantify UV-mediated epidermal cell damage and the degree of i mmune photoprotection provided by various agents.