Di Nuzzo S, Sylva-Steenland R M, de Rie M A, Das P K, Bos J D, Teunissen M B
Department of Dermatology, Academic Medical Center, University of Amsterdam, The Netherlands.
J Invest Dermatol. 1998 Jun;110(6):978-81. doi: 10.1046/j.1523-1747.1998.00220.x.
Acute, low-doses of ultraviolet (UV)-B radiation affect the immune competent cells of the skin immune system. In this study, we examined the time-dependent changes of the cutaneous T cell population in normal human volunteers following a single local exposure to UV. Solar-simulated UV radiation caused an initial decrease in intraepidermal T cell numbers, even leading to T cell depletion at day 4, whereupon a considerable infiltration of T cells in the epidermis occurred that peaked at day 14. In the dermis the number of T cells was markedly increased at days 2 (peak) and 4 after irradiation, and subsequently declined to the nonirradiated control values at day 10. Double-staining with several T cell markers showed that the T cells, infiltrating the (epi)dermis upon UV exposure, were almost exclusively CD4+ CD45RO+ T cells, expressing an alpha/beta type T cell receptor, but lacking the activation markers HLA-DR, VLA-1, and IL-2R. Application of UVB radiation resulted in similar dynamics of T cells, indicating that the UVB wavelengths within the solar-simulated UV radiation were responsible for the selective influx of CD4+ T cells. In conjunction with UVB-induced alterations in the type and function of antigen-presenting cells (i.e., Langerhans cells and macrophages), the changes of the cutaneous T cell population may also contribute to UVB-induced immunosuppression at skin level in man.
急性低剂量紫外线B辐射会影响皮肤免疫系统的免疫活性细胞。在本研究中,我们检测了正常人类志愿者单次局部暴露于紫外线后皮肤T细胞群体随时间的变化。模拟太阳光的紫外线辐射导致表皮内T细胞数量最初减少,甚至在第4天导致T细胞耗竭,随后表皮中出现大量T细胞浸润,并在第14天达到峰值。在真皮中,照射后第2天(峰值)和第4天T细胞数量显著增加,随后在第10天降至未照射对照值。用几种T细胞标志物进行双重染色显示,紫外线暴露后浸润(表)皮的T细胞几乎全是CD4+CD45RO+T细胞,表达α/β型T细胞受体,但缺乏活化标志物HLA-DR、VLA-1和IL-2R。紫外线B辐射的应用导致T细胞出现类似的动态变化,表明模拟太阳光的紫外线辐射中的紫外线B波长是CD4+T细胞选择性流入的原因。结合紫外线B诱导的抗原呈递细胞(即朗格汉斯细胞和巨噬细胞)类型和功能的改变,皮肤T细胞群体的变化也可能导致人类皮肤水平上紫外线B诱导的免疫抑制。