Mittelbrunn María, Tejedor Reyes, de la Fuente Hortensia, García-López M Angeles, Ursa Angeles, Peñas Pablo F, García-Díez Amaro, Alonso-Lebrero José Luis, Pivel Juan Pablo, González Salvador, Gonzalez-Amaro Roberto, Sánchez-Madrid Francisco
Servicio de Inmunología, Hospital de la Princesa Universidad Autónoma de Madrid, Madrid, Spain.
J Invest Dermatol. 2005 Aug;125(2):334-42. doi: 10.1111/j.0022-202X.2005.23824.x.
Exposure to ultraviolet (UV) light induces immunosuppression. Different evidences indicate that this phenomenon is mainly a consequence of the effect of UV light on skin dendritic cells (DC). To investigate the cellular and molecular basis of this type of immunosuppression, we assessed in vitro the effect of solar-simulated UV radiation on the phenotypic and functional characteristics of human monocyte-derived DC and Langerhans-like DC. UV radiation induced a decreased expression of molecules involved in antigen capture as DC-SIGN and the mannose receptor. This effect was accompanied by a diminished endocytic capacity, an enhanced expression of molecules involved in antigen presentation such as major histocompatibility complex-II and CD86, and a significant increase in their capability to stimulate T cells. Furthermore, irradiated DC failed to acquire a full mature phenotype upon treatment with lipopolysaccharide. On the other hand, solar-simulated radiation induced the secretion of tumor necrosis factor-alpha and interleukin (IL)-10 by DC, but no IL-12. Interestingly, solar-simulated UV radiation also caused an altered migratory phenotype, with an increased expression of CXCR4, and a lack of induction of CCR7, thus correlating with a high chemotactic response to stromal cell-derived factor 1(SDF-1) (CXCL12), but not to secondary lymphoid tissue chemokine (SLC) (CCL21). These data indicate that solar-simulated UV radiation induces a defective maturation and an anomalous migratory phenotype of DC.
暴露于紫外线（UV）会导致免疫抑制。不同的证据表明，这种现象主要是紫外线对皮肤树突状细胞（DC）作用的结果。为了研究这种免疫抑制类型的细胞和分子基础，我们在体外评估了模拟太阳紫外线辐射对人单核细胞衍生的DC和朗格汉斯样DC的表型和功能特性的影响。紫外线辐射导致参与抗原捕获的分子如DC-SIGN和甘露糖受体的表达降低。这种效应伴随着内吞能力的减弱、参与抗原呈递的分子如主要组织相容性复合体-II和CD86的表达增强，以及它们刺激T细胞能力的显著增加。此外，经脂多糖处理后，受辐射的DC未能获得完全成熟的表型。另一方面，模拟太阳辐射诱导DC分泌肿瘤坏死因子-α和白细胞介素（IL）-10，但不分泌IL-12。有趣的是，模拟太阳紫外线辐射还导致迁移表型改变，CXCR4表达增加，且未诱导CCR7，因此与对基质细胞衍生因子1（SDF-1）（CXCL12）的高趋化反应相关，但与对二级淋巴组织趋化因子（SLC）（CCL21）的趋化反应无关。这些数据表明，模拟太阳紫外线辐射诱导DC成熟缺陷和异常迁移表型。
