McFadden N, Larsen T E
Photodermatol. 1986 Feb;3(1):36-40.
Experimental induction of PLME lesions in 22 patients, using a pure, high-intensity UVA light source is reported. Fourteen patients had a reduced MED value for either UVB (11 patients) and/or UVA (7 patients). The UVA-SUN 2000 dose required to provoke a positive PLME reaction varied from 26 to 104 J/cm2. The small papular PMLE-type patients were shown to be more photosensitive and the UVA provocation doses required exceeded 50 J/cm2 in 20/22 patients. Lesional immunoglobulin deposition along the BMZ was seen in 3 patients while lesional BMZ complement deposits occurred in 9/15 patients, 2 of whom had similar findings in the dermal capillaries. Complement deposition occurred in non-irradiated control sites in 4 patients. The immunohistologic findings, for reasons given, fail to support the hypothesis of an immune cell-mediated response as the primary event in the pathogenesis of PMLE.
据报道，使用纯净的高强度UVA光源对22例患者进行了光线性类弹力纤维病（PLME）损伤的实验性诱导。14例患者的中波紫外线（UVB，11例患者）和/或长波紫外线（UVA，7例患者）的最小红斑量（MED）值降低。引发阳性PLME反应所需的UVA - SUN 2000剂量在26至104 J/cm²之间变化。小丘疹型PMLE患者表现出更高的光敏性，22例患者中有20例引发反应所需的UVA激发剂量超过50 J/cm²。3例患者在病变部位的基底膜带（BMZ）可见免疫球蛋白沉积，而15例患者中有9例在病变部位的BMZ出现补体沉积，其中2例在真皮毛细血管有类似表现。4例患者在未照射的对照部位出现补体沉积。由于所述原因，免疫组织学结果不支持免疫细胞介导的反应是PMLE发病机制中的主要事件这一假说。
