Clingen P H, Berneburg M, Petit-Frère C, Woollons A, Lowe J E, Arlett C F, Green M H
CRC Drug--DNA Interaction Research Group, Department of Oncology, University College London Medical School, 91 Riding House Street, London W1P 8BT, UK.
Br J Dermatol. 2001 Jul;145(1):54-62. doi: 10.1046/j.1365-2133.2001.04281.x.
Recent studies have demonstrated that a tanning lamp emitting predominantly ultraviolet (UV) A induces significant yields of the type of potentially mutagenic DNA damage that are associated with the onset of skin cancer (i.e. cyclobutane pyrimidine dimers). UV-induced immunosuppression is also an important event leading to skin cancer.
To the modulation of key immunological molecules following exposure to a broad-spectrum UVB lamp and a predominantly UVA-emitting tanning lamp using model in vitro systems.
We compared secretion and mRNA expression of interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha in normal human epidermal keratinocytes, and interferon (IFN)-gamma-induced intracellular adhesion molecule (ICAM)-1 in normal human fibroblasts irradiated in vitro with a broad-spectrum UVB lamp or with a Philips 'Performance' tanning lamp.
With broad-spectrum UVB irradiation, upregulation of IL-6 and TNF-alpha mRNA was detected 6 h after irradiation, and a dose-dependent increase of cytokines in the supernatants of irradiated cells was found 24 h after irradiation. In contrast, there was no cytokine secretion and little evidence for mRNA upregulation following exposure to a tanning lamp. When cells were exposed first to broad-spectrum UVB, then the tanning lamp, UVB-induced cytokine secretion was inhibited, although mRNA levels were upregulated to a level close to that observed with UVB alone. By using a Schott WG 320 nm filter to attenuate the level of UVB relative to UVA emitted by the tanning lamp, the inhibition of cytokine secretion was shown to be associated with UVA exposure. Both UV sources inhibited IFN-gamma-induced ICAM-1 mRNA expression in a dose-dependent fashion. By using a Schott WG 335 nm filter, inhibition of ICAM-1 mRNA expression by the tanning lamp was shown to be associated with UVB exposure.
These results suggest that UV sources emitting different levels of UVA and UVB have differential effects on the modulation of different immunoregulatory molecules, and indicate that there are potential interactions between these wavelengths.
近期研究表明，主要发射紫外线（UV）A的晒黑灯可诱导产生大量与皮肤癌发生相关的潜在诱变DNA损伤（即环丁烷嘧啶二聚体）。紫外线诱导的免疫抑制也是导致皮肤癌的一个重要事件。
利用体外模型系统，研究暴露于广谱UVB灯和主要发射UVA的晒黑灯后关键免疫分子的调节情况。
我们比较了正常人表皮角质形成细胞中白细胞介素（IL）-6和肿瘤坏死因子（TNF）-α的分泌及mRNA表达，以及正常人成纤维细胞中干扰素（IFN）-γ诱导的细胞间黏附分子（ICAM）-1的表达，这些细胞在体外分别用广谱UVB灯或飞利浦“Performance”晒黑灯照射。
经广谱UVB照射后，照射6小时检测到IL-6和TNF-α mRNA上调，照射24小时后发现照射细胞上清液中细胞因子呈剂量依赖性增加。相比之下，暴露于晒黑灯后未检测到细胞因子分泌，且几乎没有mRNA上调的证据。当细胞先暴露于广谱UVB，然后再暴露于晒黑灯时，UVB诱导的细胞因子分泌受到抑制，尽管mRNA水平上调至接近单独使用UVB时观察到的水平。通过使用肖特WG 320 nm滤光片降低晒黑灯发射的UVB相对于UVA的水平，结果表明细胞因子分泌的抑制与UVA暴露有关。两种紫外线源均以剂量依赖性方式抑制IFN-γ诱导的ICAM-1 mRNA表达。通过使用肖特WG 335 nm滤光片，发现晒黑灯对ICAM-1 mRNA表达的抑制与UVB暴露有关。
这些结果表明，发射不同水平UVA和UVB的紫外线源对不同免疫调节分子的调节具有不同作用，并表明这些波长之间存在潜在相互作用。
