AA patients have a higher incidence of various T-cell-driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over-activation of skin-homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using AA as a model disease, our approach of intra-individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities.

The aim of this study was to evaluate, in vitro, the protective effects of taurine, omega3/6 and a mixture of tocotrienols, tocomonoenol and tocopherol (DVL 95), in UVB-irradiated keratinocytes. For this purpose, immortalized human keratinocytes were pre-incubated for 2h with the above mentioned substances, singularly or in combination, and irradiated with UVB 60 mJ/cm 2 . Both, UVB dose and substance concentrations, have been selected after multiple cell viability experiments. Their possible protective effect was explored analyzing p-53 levels at 24h after UVB irradiation. Our results showed that the tested substances displayed significant cytoprotective properties. In particular, these compounds when used synergistically resulted more effective in reducing UVB-induced p-53 protein expression. Probably, their effects would be enhanced when used in combination. Since the regulation of p-53 pathway is considered an essential part of treatment in multiple inflammatory diseases, this mixture natural extracts may be an interesting option to improve or prevent UV-induced or aggravated clinical conditions. 652 Protection strategies to inhibit blue light irradiation effects in-vitro and in skin ex-vivo R Campiche, C Mendrok-Edinger, K Gadsinski, A Janssen, R Schü tz, T Rudolph, J Klock and J Vollhardt Personal Care, DSM Nutritional Products, Kaiseraugst, Switzerland The negative impacts of visible light, particularly high energy visible light (HEV) or blue light (wavelength 380-500nM), to skin are still not fully understood. A few studies have shown an increase of blue light-induced oxidative stress and hyperpigmentation in-vitro suggesting a contribution to photo-aging. Only two UV-filters were found to partially block wavelength >400nm, hence additional means of protection are needed. We investigated blue lightinduced cutaneous damages and screened for compounds to suppress these damages. Vitamins B3, B6 and E as well as Q10 could prevent beta-carotene from blue light-dependent degradation in-vitro on PMMA plates. To investigate the potential of these compounds to suppress blue light induced damages in skin, we developed an ex-vivo model of blue light irradiation. Using fluencies of up to 100J/cm 2 we could show a dose-dependent increase of reactive oxygen species (by immunofluorescent labeling), and we established protein carbonylation (by Oxyblot analysis) as a novel marker of blue light induced skin damage. We found that distinct compounds like e.g vitamin B3, lutein or Q10 as well as an extract of the green fresh water microalgae Scenedesmus rubescens could suppress blue light induced damage significantly (p<0.05). In summary, we provide evidence that blue light induces cutaneous damage via protein carbonylation, that can be suppressed by specific vitamins, Q10 and carotenoids, or algae extracts. WITHDRAWN ABSTRACTS | Photobiology and Pigmentation

In contrast to genomic data, we did not find a general difference between baseline TLR7 expression of SCC and BCC on the protein level. Nevertheless, the expression of TLR7 by the inflammatory infiltrate associated with SCC may correlate with the degree of differentiation of SCC possibly indicating better outcome.