Future Developments

Epidermal DNA is probably the molecule that converts the physical energy of UV into a biological signal, thus leading to immunodysregulation. Liposome-encapsuled T4 endonuclease V, which increases the rate of pyrimidine dimer repair, can prevent UV-induced suppression of delayed-type hypersensitivity (Yarosh et al. 1999). Thus, repair of UV radiation-induced DNA damage through topical application of DNA repair enzymes seems to be a promising approach to reverse damaging UV effects. Stege et al. (Stege et al. 2000) demonstrated that application of the DNA repair enzyme photolyase in liposomes after UV irradiation induced dimer reversal and restored normal immune status. Whereas the potential of DNA repair enzymes as adjuvants in sunscreens or after sun lotions to prevent photocarcinogenesis is obvious, the ability of these chemicals to prevent photoinduction of LE remains unclear. Since DNA damage is believed to be crucial for the initiation of UV-induced autoimmunity, this approach is worth testing in UV-induced LE. Therefore, future development of sunscreen products should take the current knowledge of the pathophysiology of UV-induced LE into consideration to achieve more specifically tailored photoprotective agents.

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