UVA-induced immunosuppression

It has previously been demonstrated that chronic low-dose solar-simulated ultraviolet (UV) radiation can induce both local and systemic immunosuppression as well as tolerance to a topically applied hapten. Epidermal cells from UV-irradiated mice inhibit spontaneous regression of tumours indicating that UV-induced immunosuppression is likely to permit the outgrowth of developing UV-induced skin tumours. We have used a chronic low-dose UV-irradiation protocol to investigate the effects of UVA on the skin immune system of C3H/HeJ mice. Irradiation with UVA + B significantly suppressed the local and systemic primary contact sensitivity (CS) response to the hapten TNCB. Furthermore UVA + B reduced Langerhans cell (LC) and dendritic epidermal T cell (DETC) numbers in chronically UV-irradiated mice. UVA-irradiation induced local, but not systemic, immunosuppression and reduced LC (32%) but not DETC from the epidermis compared to the shaved control animals. Treatment of mice with UVA + B or UVA radiation also induced an impaired secondary CS response, and this tolerance was transferable with spleen cells. Therefore exposure of C3H/HeJ mice 5 days per week for 4 weeks with UVA can induce local immunosuppression and tolerance. One of the mechanisms by which UVA affects biological systems is production of reactive oxygen species. We have also shown that Vitamin E, an inhibitor of lipid peroxidation, prevents UV-induced immunosuppression and loss of LC. It is possible that the UVA in UV radiation induces epidermal lipid peroxidation which stimulates LC migration from the epidermis, thus contributing to UV-induced immunosuppression. Hence, inhibition of epidermal lipid peroxidation by Vitamin E may provide some protection to the skin immune system from these effects of UV.