Horio T, Okamoto H
J Invest Dermatol. 1982 May;78(5):402-5. doi: 10.1111/1523-1747.ep12507561.
A suppressive effect of treatment with 8-methoxypsoralen (8-MOP) and long-wave ultraviolet light (PUVA) on the induction and elicitation of contact sensitivity to dinitrochlorbenzene was observed in guinea pigs. The mechanisms by which PUVA exerts its inhibitory effect seemed to be variable depending on the site and extent of the treatment. When PUVA was given at the induction site, only one treatment using topical 1% 8-MOP and 7,6 J/cm2 UVA is a small area was enough to inhibit sensitization, and the effect was long-lasting. This seemed to be caused by impairment of Langerhans cell function. On the other hand, when induction was attempted through nontreated skin, repeated exposures in larger areas were needed to suppress the challenge reactions. Nonspecific primary irritant dermatitis revealed a similar effect. This inhibitory effect was transient and possibly caused by lack of sufficient number of immune cells for the elicited reactions. An apparent enhancement of challenge reactions at the PUVA-treated site was too complicated to permit interpretation of its mechanism.
在豚鼠身上观察到，用8-甲氧基补骨脂素（8-MOP）和长波紫外线（PUVA）治疗对二硝基氯苯接触敏感性的诱导和激发具有抑制作用。PUVA发挥其抑制作用的机制似乎因治疗部位和范围而异。当在诱导部位给予PUVA时，在小面积上仅使用局部1% 8-MOP和7.6 J/cm² UVA进行一次治疗就足以抑制致敏，且效果持久。这似乎是由朗格汉斯细胞功能受损引起的。另一方面，当试图通过未处理的皮肤进行诱导时，则需要在更大面积上反复暴露以抑制激发反应。非特异性原发性刺激性皮炎显示出类似的效果。这种抑制作用是短暂的，可能是由于引发反应所需的免疫细胞数量不足所致。在PUVA治疗部位激发反应的明显增强情况过于复杂，难以解释其机制。
