Stoebner P E, Poosti R, Djoukelfit K, Martinez J, Meunier L
Service de Dermatologie, CHU Caremeau, Place du Pr. Debre, 30029 Nîmes cedex 09, France.
Br J Dermatol. 2007 Jun;156(6):1315-20. doi: 10.1111/j.1365-2133.2007.07895.x.
Ultraviolet (UV) exposure of human skin causes immunosuppression that contributes to the growth of skin cancer. The contribution of UVA in these processes is still a matter of debate.
The purpose of our study was first to find a dose-response effect of UVA exposure on human epidermal antigen-presenting cell (APC) activity and to evaluate the protective capacity of two sunscreen formulations against a high level of acute UVA exposure. We also tried to evaluate the protective capacity afforded by the same sunscreens against UVA-induced clinical changes such as redness and pigmentation.
The functional assessment of the alloantigen-presenting capacity of epidermal cells prepared from skin keratotome samples 3 days after UVA exposure was measured with a mixed epidermal cell-lymphocyte reaction (MECLR) in each healthy volunteer (n = 16). Redness and pigmentation were assessed by chromametry 24 h after exposure to a single UVA dose.
In vivo UVA exposure to 15, 30 and 60 J cm(-2) resulted in a dose-dependent decrease in purified allogeneic T cell (CD4+ T cells) proliferation induced by UVA-irradiated epidermal cells. The epidermal APC function was significantly decreased with a suberythemal exposure corresponding to 15 J cm(-2). The decrease, partial and not statistically different between 30 and 60 J cm(-2), exhibits a plateau-response effect. There was no correlation between the decrease of the epidermal APC function and the intensity of erythema and persistent pigment darkening. Both sunscreen formulations strongly inhibited the UVA-induced reduction of MECLR at 90 J cm(-2).
Our results clearly demonstrate that UVA impairs the APC activity of the epidermal cells and thus may contribute to UV-induced immunosuppression in humans. They also indicate that erythema and immunosuppression have different dose-response curves in the UVA range. The two sunscreen formulations afforded a significant protection against the decrease in epidermal APC activity induced by exposure to a high UVA dose (90 J cm(-2)).
紫外线(UV)照射人体皮肤会导致免疫抑制,这有助于皮肤癌的生长。UVA在这些过程中的作用仍存在争议。
我们研究的目的首先是找出UVA照射对人表皮抗原呈递细胞(APC)活性的剂量反应效应,并评估两种防晒配方对高水平急性UVA照射的保护能力。我们还试图评估相同防晒剂对UVA诱导的临床变化(如发红和色素沉着)的保护能力。
在每位健康志愿者(n = 16)中,用混合表皮细胞-淋巴细胞反应(MECLR)测量UVA照射3天后从皮肤切片样本制备的表皮细胞的同种异体抗原呈递能力的功能评估。在暴露于单一UVA剂量24小时后,通过色度法评估发红和色素沉着。
体内UVA暴露于15、30和60 J/cm²导致UVA照射的表皮细胞诱导的纯化同种异体T细胞(CD4 + T细胞)增殖呈剂量依赖性降低。表皮APC功能在对应于15 J/cm²的亚红斑暴露下显著降低。在30和60 J/cm²之间的降低是部分的且无统计学差异,呈现出平台反应效应。表皮APC功能的降低与红斑强度和持续性色素沉着加深之间没有相关性。两种防晒配方在90 J/cm²时均强烈抑制UVA诱导的MECLR降低。
我们的结果清楚地表明,UVA会损害表皮细胞的APC活性,因此可能导致人类紫外线诱导的免疫抑制。它们还表明,在UVA范围内,红斑和免疫抑制具有不同的剂量反应曲线。两种防晒配方对暴露于高UVA剂量(90 J/cm²)引起的表皮APC活性降低提供了显著的保护。