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UVA-induced immune suppression in human skin: protective effect of vitamin E in human epidermal cells in vitro
P Clement-Lacroix1, L Michel, A Moysan
1Laboratoire de Dermatologie, INSERM U312, Hôpital Saint-Louis, Paris, France.
Abstract:
UVA (320-400 nm) radiation damage to membranes, proteins, DNA and other cellular targets is predominantly related to oxidative processes. In the present study, we demonstrated that cutaneous UVA-induced immunosuppression can be related, at least in part, to the appearance of these oxidative processes. The UVA-induced oxidative processes in freshly isolated epidermal cells were monitored by measuring the thiobarbituric 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 reaction (MECLR). In addition, the effects of a potent antioxidant (vitamin E) on these two UVA-induced processes were analysed. Our results showed that the antigen-presenting function of Langerhans cells measured in the MECLR is dose-dependently decreased by UVA radiation (up to 20J/cm2). Overnight incubation of epidermal cells with vitamin E (400 mumol/l) before irradiation partially protected epidermal cells from the immunosuppressive effects of UVA radiation, and decreased TBARS release into the supernatant (a decrease of 35% compared with a control without vitamin E). Our results suggest that UVA radiation may alter cell-presenting antigen function partly via the generation of reactive oxygen species which trigger peroxidative processes, and these data contribute to the understanding of the role of oxidative mechanisms in immune suppression induced by UVA radiation. Our in vitro model can be used to quantify UV-mediated epidermal cell damage and the degree of immune photoprotection provided by various agents.
Insights
Ultraviolet A (UVA) radiation causes skin immune suppression through oxidative processes. Vitamin E partially protected against UVA-induced damage by reducing peroxidation and preserving Langerhans cell function.
Area of Science:
- Dermatology
- Immunology
- Oxidative Stress
Background:
- Ultraviolet A (UVA) radiation induces cellular damage primarily through oxidative processes.
- Cutaneous UVA exposure can lead to immunosuppression, but the underlying mechanisms require further elucidation.
Purpose of the Study:
- To investigate the role of oxidative processes in UVA-induced immunosuppression.
- To assess the protective effects of vitamin E against UVA-induced skin immune damage.
Main Methods:
- Monitoring UVA-induced oxidative stress using thiobarbituric acid reactive substances (TBARS) assay.
- Evaluating UVA's effect on allogeneic lymphocyte proliferation in mixed epidermal cell-lymphocyte reaction (MECLR).
- Assessing vitamin E's impact on UVA-induced TBARS release and MECLR function.
Main Results:
- UVA radiation dose-dependently impaired the antigen-presenting function of Langerhans cells in MECLR.
- Vitamin E pre-treatment partially protected epidermal cells from UVA-induced immunosuppression.
- Vitamin E significantly reduced UVA-induced TBARS release by 35%.
Conclusions:
- UVA radiation alters antigen-presenting cell function partly through reactive oxygen species generation and peroxidation.
- Oxidative mechanisms play a significant role in UVA-induced immune suppression.
- An in vitro model was established to quantify UV-induced epidermal damage and photoprotection.