Soter N A
Department of Dermatology, New York University School of Medicine, NY 10016.
Semin Dermatol. 1990 Mar;9(1):11-5.
The responses of normal skin to ultraviolet (UV) irradiation are an example of inflammation. The chromophores initiating the reaction are unknown. Characteristic clinical findings are erythema, heat, swelling, and pain. Histopathologic changes include epidermal keratinocyte damage with Langerhans cell depletion and dermal edema, endothelial swelling, mast cell degranulation, and cellular infiltration with neutrophils and monocytes. Biochemical changes include release of histamine, cyclo-oxygenase, and lipoxygenase-derived products of arachidonic acid, kinins, and cytokines, probably from a range of epidermal and dermal cell types. These substances very likely assist in mediation of the reaction. The response is more pronounced in young subjects. UVB (280 to 315 nm) and UVA (315 to 400 nm) radiation both produce inflammation, but with marked qualitative and quantitative differences. UVB having more effect on the epidermis, UVA more on the dermis.
正常皮肤对紫外线(UV)照射的反应是炎症的一个例子。引发该反应的发色团尚不清楚。典型的临床症状包括红斑、发热、肿胀和疼痛。组织病理学变化包括表皮角质形成细胞损伤伴朗格汉斯细胞减少以及真皮水肿、内皮细胞肿胀、肥大细胞脱颗粒,还有中性粒细胞和单核细胞的细胞浸润。生化变化包括组胺、环氧化酶以及花生四烯酸经脂氧合酶衍生的产物、激肽和细胞因子的释放,这些物质可能来自多种表皮和真皮细胞类型。这些物质很可能有助于介导该反应。该反应在年轻受试者中更为明显。紫外线B(280至315纳米)和紫外线A(315至400纳米)辐射均可产生炎症,但在性质和数量上存在显著差异。紫外线B对表皮的影响更大,紫外线A对真皮的影响更大。