Kölgen Wendy, van Meurs Marjan, Jongsma Marjan, van Weelden Huib, Bruijnzeel-Koomen Carla A F M, Knol Edward F, van Vloten Willem A, Laman Jon, de Gruijl Frank R
Department of Dermatology, University Medical Center Utrecht, Utrecht.
Arch Dermatol. 2004 Mar;140(3):295-302. doi: 10.1001/archderm.140.3.295.
Disturbances in UV-induced Langerhans cell migration and T helper (T(H)) 2 cell responses could be early steps in the pathogenesis of PLE.
To establish whether UV-B exposure induces aberrant cytokine expression in the uninvolved skin of patients with polymorphous light eruption (PLE).
Immunohistochemical staining and comparison of microscopic sections of skin irradiated with 6 times the minimal dose of UV-B causing erythema and the unirradiated skin of patients with PLE and of healthy individuals.
University Medical Center (Dutch National Center for Photodermatoses). Patients Patients with PLE (n = 6) with clinically proven pathological responses to UV-B exposure and normal erythemal sensitivity. Healthy volunteers (n = 5) were recruited among students and hospital staff.
Expression of cytokines related to Langerhans cell migration (interleukin [IL] 1, IL-18,and tumor necrosis factor [TNF] alpha); T(H)2 responses (IL-4 and IL-10); and T(H)1 responses (IL-6, IL-12, and interferon gamma). Double staining was performed for elastase (neutrophils), tryptase (mast cells), and CD36 (macrophages).
The number of cells expressing IL-1beta and TNF-alpha was reduced in the UV-B-exposed skin of patients with PLE compared with the skin of healthy individuals (P<.05 for TNF-alpha). No differences were observed in the expression of T(H)1-related cytokines but fewer cells expressing IL-4 infiltrated the epidermis of patients with PLE 24 hours after irradiation (P =.03). After UV exposure TNF-alpha, IL-4, and, to a lesser extent, IL-10 were predominantly expressed by neutrophils.
The reduced expression of TNF-alpha, IL-4, and IL-10 in the UV-B-irradiated skin of patients with PLE appears largely attributable to a lack of neutrophils, and is indicative of reduced Langerhans cell migration and reduced T(H)2 skewing. An impairment of these mechanisms underlying UV-B-induced immunosuppression may be important in the pathogenesis of PLE.
紫外线诱导的朗格汉斯细胞迁移和辅助性T（Th）2细胞反应紊乱可能是多形性日光疹（PLE）发病机制的早期步骤。
确定紫外线B（UV-B）照射是否会在多形性日光疹（PLE）患者未受累皮肤中诱导细胞因子表达异常。
对接受引起红斑的最小剂量6倍的UV-B照射的皮肤以及PLE患者和健康个体的未照射皮肤的显微切片进行免疫组织化学染色和比较。
大学医学中心（荷兰国家光皮肤病中心）。患者：经临床证实对UV-B照射有病理反应且红斑敏感性正常的PLE患者（n = 6）。健康志愿者（n = 5）从学生和医院工作人员中招募。
与朗格汉斯细胞迁移相关的细胞因子（白细胞介素[IL]1、IL-18和肿瘤坏死因子[TNF]α）；Th2反应（IL-4和IL-10）；以及Th1反应（IL-6、IL-12和干扰素γ）的表达。对弹性蛋白酶（中性粒细胞）、类胰蛋白酶（肥大细胞）和CD36（巨噬细胞）进行双重染色。
与健康个体的皮肤相比，PLE患者接受UV-B照射的皮肤中表达IL-1β和TNF-α的细胞数量减少（TNF-α，P<.05）。在Th1相关细胞因子的表达上未观察到差异，但照射后24小时，浸润PLE患者表皮的表达IL-4的细胞较少（P = 0.03）。紫外线照射后，TNF-α、IL-4以及在较小程度上IL-10主要由中性粒细胞表达。
PLE患者接受UV-B照射的皮肤中TNF-α、IL-4和IL-10表达降低似乎主要归因于中性粒细胞的缺乏，这表明朗格汉斯细胞迁移减少和Th2偏向性降低。这些UV-B诱导的免疫抑制潜在机制的损害可能在PLE的发病机制中起重要作用。
