Dandie G W, Clydesdale G J, Jacobs I, Muller H K
Division of Pathology, University of Tasmania, Hobart, Australia.
Mutat Res. 1998 Nov 9;422(1):147-54. doi: 10.1016/s0027-5107(98)00186-9.
Depletion of epidermal Langerhans cells (LC) and the concomitant depression of the skin immune system after excessive exposure to ultraviolet B light (UVB) has been established in the international literature for some time. Our investigations were intended to determine whether or not these phenomena occurred as a direct result of increased LC migration being triggered by the UVB exposure. To test this hypothesis, a sheep model was established in which the lymphatic vessels draining a defined region of skin were cannulated and the cells migrating towards the regional lymph node continuously collected. Cell populations in these collections were identified and enumerated by indirect immunofluorescence and flow cytometry. These experiments showed there was a significant, dose-dependent increase in the rate of LC migration from sheep skin after exposure to doses of UVB light exceeding 1 minimal erythemal dose (MED). In a series of parallel experiments, the functional characteristics of dendritic cells (DC) migrating from normal or UVB irradiated sheep were studied. To assay them, enriched preparations of DC were collected via cannulated afferent lymphatic vessels and pulsed with antigen prior to incubation with autologous peripheral blood lymphocytes. The relative efficiency of antigen presentation was determined by the ability of DC to induce T cell proliferation. Our data clearly demonstrate that there is a profound loss of normal antigen-presenting cell function after exposure to UVB light. Various experiments were undertaken to determine the mechanism(s) associated with these changes in migration kinetics and cellular function. Electron microscopic examinations of LC migrating from normal or UVB irradiated skin have demonstrated a profound loss of dendritic processes after UVB exposure. This provides a possible explanation for the changes in skin immunity after UVB exposure.
一段时间以来，国际文献已经证实，过度暴露于中波紫外线（UVB）后，表皮朗格汉斯细胞（LC）会减少，同时皮肤免疫系统也会受到抑制。我们的研究旨在确定这些现象是否是由于UVB暴露引发LC迁移增加的直接结果。为了验证这一假设，建立了一个绵羊模型，在该模型中，将引流特定皮肤区域的淋巴管插管，并持续收集向区域淋巴结迁移的细胞。通过间接免疫荧光和流式细胞术对这些收集物中的细胞群体进行鉴定和计数。这些实验表明，暴露于超过1个最小红斑量（MED）的UVB剂量后，绵羊皮肤中LC的迁移速率显著增加，且呈剂量依赖性。在一系列平行实验中，研究了从正常或UVB照射的绵羊迁移而来的树突状细胞（DC）的功能特性。为了对它们进行检测，通过插管的输入淋巴管收集富集的DC制剂，并在与自体外周血淋巴细胞孵育之前用抗原脉冲处理。通过DC诱导T细胞增殖的能力来确定抗原呈递的相对效率。我们的数据清楚地表明，暴露于UVB后，正常抗原呈递细胞功能会严重丧失。进行了各种实验以确定与迁移动力学和细胞功能这些变化相关的机制。对从正常或UVB照射皮肤迁移而来的LC进行电子显微镜检查，结果显示UVB暴露后树突状突起严重丧失。这为UVB暴露后皮肤免疫的变化提供了一种可能的解释。
