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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >An action spectrum (290-320 nm) for TNFa protein in human skin in vivo suggests that basal-layer epidermal DNA is the chromophore
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An action spectrum (290-320 nm) for TNFa protein in human skin in vivo suggests that basal-layer epidermal DNA is the chromophore

机译：人体皮肤中TNFa蛋白的作用谱（290-320 nm）表明，基底层表皮DNA是发色团

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摘要

Terrestrial solar UVB radiation (≈ 295-320 nm) readily induces cyclobutane pyrimidine dimers (CPDs) in human skin DNA that result in characteristic mutations associated with nonmelanoma skin cancer. The proinflammatory cytokine TNFa is important in mouse skin chemical carcinogenesis and is thought to also play a role in UVR-induced skin cancer by its immunomodulatory properties. There is some in vitro evidence that CPDs initiate the production of TNFα, and we tested this hypothesis by comparing the wavelength dependence (action spectrum) for TNFα protein induction in human skin in vivo with our earlier in vivo action spectra for CPD induction in four different epidermal layers of human skin. Normal volunteers (n = 35) were irradiated with physiologically relevant doses of monochromatic UVB (290-320 nm), and TNFα concentration was assessed, by high-sensitivity ELISA, in exudates from skin suction blisters raised 8 h after irradiation. An action spectrum, constructed from the slopes of the dose-response curves at the different wavelengths, showed maximal efficacy at 300 nm. An excellent match was observed for TNFα and the CPD action spectrum for cells in the lower basal epidermis. These data strongly suggest that UVB-induced photodamage to DNA in the epidermal basal layer is a major trigger for TNFα production. The TNFα may originate directly from the keratino-cytes in this layer or inflammatory cells that are rapidly recruited into the upper dermis (e.g., neutrophils) as a consequence of DNA photodamage to basal-layer keratinocytes.
机译：陆地太阳紫外线辐射（≈295-320 nm）容易在人皮肤DNA中诱导环丁烷嘧啶二聚体（CPD），从而导致与非黑素瘤皮肤癌相关的特征性突变。促炎细胞因子TNFa在小鼠皮肤化学致癌作用中很重要，并且由于其免疫调节特性，还被认为在UVR诱导的皮肤癌中也起作用。有一些体外证据表明CPD会引发TNFα的产生，我们通过在四种不同的情况下比较人体皮肤中TNFα蛋白诱导的波长依赖性（作用谱）与我们较早的CPD诱导的体内作用谱来验证了这一假设。人皮肤的表皮层。正常志愿者（n = 35）接受生理学相关剂量的单色UVB（290-320 nm）照射，并通过高灵敏度ELISA评估照射后8 h产生的皮肤吸水疱渗出液中的TNFα浓度。由在不同波长下的剂量反应曲线的斜率构成的作用谱显示出在300 nm处的最大功效。观察到下基底表皮细胞的TNFα和CPD作用谱非常匹配。这些数据强烈表明，UVB诱导的对表皮基底层中DNA的光损伤是TNFα产生的主要诱因。 TNFα可能直接来源于该层的角质形成细胞或由于对基质层角质形成细胞的DNA光损伤而迅速募集到上层真皮（例如中性粒细胞）中的炎症细胞。

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