Steerenberg Peter A, Daamen Frieda, Weesendorp Eefke, Van Loveren Henk
Laboratory for Toxicology, Pathology and Genetics, National Institute for Public Health and the Environment, P.O. Box 1, 3720 BA Bilthoven, The Netherlands.
J Photochem Photobiol B. 2006 Jul 3;84(1):28-37. doi: 10.1016/j.jphotobiol.2006.01.009. Epub 2006 Feb 28.
It is well known that ultraviolet (UV) radiation induces erythema, immunosuppression and carcinogenesis. We hypothesized that chronic exposure to solar UV radiation induces adaptation that eventually prevents the suppression of acquired immunity. We studied adaptation for UV-induced immunosuppression after chronic exposure of mice to a suberythemal dose of solar simulated radiation (SSR) with Cleo Natural lamps, and subsequent exposure to an immunosuppressive dose of solar or UVB radiation (TL12). After UV dosing, the mice were sensitized and challenged with either diphenylcyclopropenone (DPCP) or picryl chloride (PCl). To assess the adaptation induced by solar simulated radiation, we measured the proliferative response and cytokine production of skin-draining lymph node cells after immunization to DPCP, the contact hypersensitivity (CHS) response to PCl, and thymine-thymine (T-T) cyclobutane dimers in the skin of mice. After induction of immunosuppression by SSR or by TL12 lamps, the proliferative response of draining lymph node cells after challenge with DPCP, or the CHS after challenge with PCl, showed significant suppression of the immune response. Chronic irradiation from SSR preceding the immunosuppressive dose of UV failed to restore the suppressed immune response. Reduced lipopolysaccharide-triggered cytokine production (of IL-12p40, IFN-gamma, IL-6 and TNF-alpha) by draining lymph node cells of mice sensitized and challenged with DPCP indicated that no adaptation is induced. In addition, the mice were not protected from T-T dimer DNA damage after chronic solar irradiation. Our studies reveal no evidence that chronic exposure to low doses of SSR induces adaptation to UV-induced suppression of acquired immunity.
众所周知，紫外线（UV）辐射可诱发红斑、免疫抑制和致癌作用。我们推测，长期暴露于太阳紫外线辐射会引发适应性变化，最终防止获得性免疫受到抑制。我们使用Cleo Natural灯，对小鼠进行亚红斑剂量的太阳模拟辐射（SSR）长期照射，随后再给予免疫抑制剂量的太阳辐射或UVB辐射（TL12），以此研究紫外线诱导的免疫抑制的适应性。紫外线照射后，用二苯基环丙烯酮（DPCP）或苦味酸氯（PCl）对小鼠进行致敏和激发。为评估太阳模拟辐射诱导的适应性，我们测量了免疫DPCP后皮肤引流淋巴结细胞的增殖反应和细胞因子产生、对PCl的接触性超敏反应（CHS）以及小鼠皮肤中的胸腺嘧啶-胸腺嘧啶（T-T）环丁烷二聚体。在用SSR或TL12灯诱导免疫抑制后，用DPCP激发后引流淋巴结细胞的增殖反应，或用PCl激发后的CHS，均显示免疫反应受到显著抑制。在给予免疫抑制剂量的紫外线之前，由SSR进行的长期照射未能恢复受抑制的免疫反应。用DPCP致敏和激发的小鼠的引流淋巴结细胞中，脂多糖触发的细胞因子产生（IL-12p40、IFN-γ、IL-6和TNF-α）减少，表明未诱导适应性变化。此外，长期太阳照射后，小鼠并未免受T-T二聚体DNA损伤。我们的研究没有发现证据表明长期暴露于低剂量的SSR会诱导对紫外线诱导的获得性免疫抑制的适应性。
