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与对照组相比,紫外线辐射对多形性日光疹患者造成的免疫抑制作用较小。

Ultraviolet radiation causes less immunosuppression in patients with polymorphic light eruption than in controls.

作者信息

Palmer Roy A, Friedmann Peter S

机构信息

Department of Dermatopharmacology, Southampton General Hospital, Southampton, UK.

出版信息

J Invest Dermatol. 2004 Feb;122(2):291-4. doi: 10.1046/j.0022-202X.2004.22213.x.

Abstract

It is hypothesized that polymorphic light eruption is characterized by a partial failure of ultraviolet radiation-induced immunosuppression, resulting in a delayed-type hypersensitivity response to photo-induced antigens. We aimed to study the susceptibility of PLE patients to UVR-induced immunosuppression, by measuring the strength of sensitization to 2,4-dinitrochlorobenzene after UVR exposure, and to diphenylcyclopropenone without UVR exposure, in subjects with PLE and controls. Thirteen PLE patients and 11 controls were exposed to 1 minimum erythema dose (MED) of UVR delivered from Waldmann UV-6 bulbs to the upper inner arm. Twenty-four hours later at the same site they were exposed to a sensitizing dose of 2,4-dinitrochlorobenzene. One week later they were exposed to a sensitizing dose of diphenylcyclopropenone at a nonirradiated site. Three weeks later all subjects were challenged with four doses of 2,4-dinitrochlorobenzene and four doses of diphenylcyclopropenone. The resulting increase in skin thickness was measured with Harpenden callipers and summed over the four doses, to give a single value representing the reactivity of the subject to 2,4-dinitrochlorobenzene (Sigma DN) and diphenylcyclopropenone (Sigma DP). Among all subjects, there was a very strong correlation between Sigma DN and Sigma DP (Pearson correlation 0.56, p=0.004). The strength of the reaction to 2,4-dinitrochlorobenzene relative to the reaction to diphenylcyclopropenone was significantly greater among PLE patients than controls (p=0.04 independent samples t test of Sigma DP-Sigma DN). We conclude that induction of sensitization by 2,4-dinitrochlorobenzene is suppressed less by UVR in patients with PLE than in healthy controls.

摘要

据推测,多形性日光疹的特征是紫外线辐射诱导的免疫抑制部分失效,从而导致对光诱导抗原的迟发型超敏反应。我们旨在通过测量多形性日光疹患者和对照组在紫外线暴露后对2,4-二硝基氯苯的致敏强度,以及在无紫外线暴露情况下对二苯环丙烯酮的致敏强度,来研究多形性日光疹患者对紫外线诱导免疫抑制的易感性。13名多形性日光疹患者和11名对照者的上臂内侧接受了来自Waldmann UV-6灯泡的1个最小红斑量(MED)的紫外线照射。24小时后,在同一部位对他们进行2,4-二硝基氯苯致敏剂量的处理。一周后,在未照射部位对他们进行二苯环丙烯酮致敏剂量的处理。三周后,对所有受试者用四剂2,4-二硝基氯苯和四剂二苯环丙烯酮进行激发试验。用Harpenden卡尺测量由此导致的皮肤厚度增加,并将四剂的测量值相加,得出一个代表受试者对2,4-二硝基氯苯(Sigma DN)和二苯环丙烯酮(Sigma DP)反应性的单一数值。在所有受试者中,Sigma DN和Sigma DP之间存在非常强的相关性(Pearson相关性为0.56,p = 0.004)。与对照组相比,多形性日光疹患者对2,4-二硝基氯苯的反应强度相对于对二苯环丙烯酮的反应强度明显更大(Sigma DP - Sigma DN的独立样本t检验,p = 0.04)。我们得出结论,与健康对照组相比,紫外线对多形性日光疹患者中2,4-二硝基氯苯诱导致敏的抑制作用较小。

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