UV Radiation Induces the Epidermal Recruitment of Dendritic Cells that Compensate for the Depletion of Langerhans Cells in Human Skin
UV Radiation Induces the Epidermal Recruitment of Dendritic Cells that Compensate for the Depletion of Langerhans Cells in Human Skin
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DOI：
10.1038/jid.2015.118
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发表时间：
2015-08-01
影响因子：
6.5
通讯作者：
Gueniche, Audrey
中科院分区：
文献类型：
--
作者：
Achachi, Amine;Vocanson, Marc;Gueniche, Audrey
紫外线会导致皮肤损伤和炎症，导致免疫功能受损并增加皮肤癌风险。朗格汉斯细胞 (LC) 是表皮的免疫哨兵，在单次 UVR 照射后几天内就会耗尽，并且可以由循环单核细胞重建。然而，导致正常 LC 库恢复的分化途径仍不清楚。为了研究紫外线损伤下人体皮肤的动态变化，我们将 29 名健康人类志愿者暴露在临床相关剂量的紫外线下，并分析了连续表皮活检中白细胞和树突状细胞 (DC) 亚群的变化。紫外线诱导的 CD1a(高) LC 消耗通过各种表皮白细胞的连续出现得到补偿。 CD14(+)单核细胞早在暴露后第1天就被招募，随后招募了两个可能代表LC前体的炎症DC亚群。这些CD1a（低）CD207（-）和迄今为止未知的CD1a（低）CD207（+）DC分别出现在UVR后第1天和第4天，并且被赋予与LC类似的T细胞激活特性。我们得出的结论是，单核细胞和炎症 DC 的募集似乎是表皮的一种生理反应，目的是修复 UVR 诱导的与免疫抑制相关的 LC 耗竭。
UVR causes skin injury and inflammation, resulting in impaired immune function and increased skin cancer risk. Langerhans cells (LCs), the immune sentinels of the epidermis, are depleted for several days following a single UVR exposure and can be reconstituted from circulating monocytes. However, the differentiation pathways leading to the recovery of a normal pool of LCs is still unclear. To study the dynamic changes in human skin with UV injury, we exposed a cohort of 29 healthy human volunteers to a clinically relevant dose of UVR and analyzed sequential epidermal biopsies for changes in leukocyte and dendritic cell (DC) subsets. UV-induced depletion of CD1a(high) LC was compensated by sequential appearance of various epidermal leukocytes. CD14(+) monocytes were recruited as early as D1 post exposure, followed by recruitment of two inflammatory DC subsets that may represent precursors of LCs. These CD1a(low) CD207(-) and the heretofore unknown CD1a(low) CD207(+) DCs appeared at day 1 and day 4 post UVR, respectively, and were endowed with T-cell-activating properties similar to those of LCs. We conclude that recruitment of monocytes and inflammatory DCs appear as a physiological response of the epidermis in order to repair UVR-induced LC depletion associated with immune suppression.