Laihia J K, Jansen C T
Department of Dermatology, University of Turku, Finland.
Eur J Immunol. 1997 Apr;27(4):984-9. doi: 10.1002/eji.1830270427.
Ultraviolet (UV) radiation impairs cutaneous immune functions and induces antigen-specific tolerance both locally at the irradiated skin site, as well as at distant skin sites and systemically. It has been postulated that in the local model, altered Langerhans' cells (LC) provide tolerogenic signals, and studies in vitro have indicated that UV radiation may down-regulate the expression of co-stimulatory molecules on the surface of these cells. To examine the effect of UV radiation on LC co-stimulatory molecules in vivo, we irradiated human volunteers with erythematogenic doses of solar-simulating UV radiation (SSR), and analyzed the expression of cell surface markers in dermatome skin samples obtained 1-72 h post-irradiation. For flow cytometric analysis, epidermal cell (EC) suspensions were prepared and double labeled with monoclonal antibodies against CD1a or HLA-DR, and B7-1 (CD80), B7-2 (CD86), ICAM-1 (CD54), ICAM-3 (CD50), LFA-3 (CD58), E-cadherin, or integrin-beta4 (CD104). In unirradiated control skin samples, keratinocytes (KC) expressed high levels of E-cadherin. LC expressed high levels of both E-cadherin and ICAM-3, and low levels of B7-2, LFA-3, ICAM-1, and integrin-beta4. Following SSR, a triphasic reaction pattern was seen: an immediate, down-regulatory phase prevailing 2-6 h post-irradiation, when the number of DR+ and CD1a+ cells were temporarily reduced; a delayed, up-regulatory phase in which the number of LC was increased and the expression intensities of CD1a, HLA-DR, B7-1, and B7-2 were strongly up-regulated, maximally evident 12-24 h after irradiation, but no more seen at 48 h; and a late phase at 72 h, in which an influx of monocytes and a concomitant rise in DR+ cells was recorded. We conclude that to understand real-life cutaneous UV immunology, studies in vitro need to be complemented with studies in vivo. In the case of LC, the effects of erythematogenic UV radiation in vivo on human LC B7 co-stimulatory molecules include an up-regulatory stage.
紫外线（UV）辐射会损害皮肤免疫功能，并在受照射的皮肤部位局部、远处皮肤部位以及全身诱导抗原特异性耐受。据推测，在局部模型中，改变的朗格汉斯细胞（LC）会提供致耐受性信号，体外研究表明紫外线辐射可能下调这些细胞表面共刺激分子的表达。为了研究紫外线辐射对体内LC共刺激分子的影响，我们用致红斑剂量的模拟太阳紫外线辐射（SSR）照射人类志愿者，并分析照射后1 - 72小时获得的皮节皮肤样本中细胞表面标志物的表达。对于流式细胞术分析，制备表皮细胞（EC）悬液，并用抗CD1a或HLA - DR以及B7 - 1（CD80）、B7 - 2（CD86）、ICAM - 1（CD54）、ICAM - 3（CD50）、LFA - 3（CD58）、E - 钙黏蛋白或整合素β4（CD104）的单克隆抗体进行双重标记。在未照射的对照皮肤样本中，角质形成细胞（KC）表达高水平的E - 钙黏蛋白。LC表达高水平的E - 钙黏蛋白和ICAM - 3，以及低水平的B7 - 2、LFA - 3、ICAM - 1和整合素β4。SSR照射后，观察到一种三相反应模式：照射后2 - 6小时出现即时下调阶段，此时DR + 和CD1a + 细胞数量暂时减少；延迟上调阶段，其中LC数量增加，CD1a、HLA - DR、B7 - 1和B7 - 2的表达强度强烈上调，在照射后12 - 24小时最为明显，但在48小时时不再出现；以及72小时的晚期阶段，其中记录到单核细胞流入和DR + 细胞随之增加。我们得出结论，为了理解实际生活中的皮肤紫外线免疫学，体外研究需要辅以体内研究。就LC而言，体内致红斑紫外线辐射对人LC B7共刺激分子的影响包括一个上调阶段。
