Tseng C, Hoffman B, Kurimoto I, Shimizu T, Schmieder G J, Taylor J R, Streilein J W
Department of Microbiology and Immunology, University of Miami School of Medicine, FL 33101.
J Invest Dermatol. 1992 Jun;98(6):871-5. doi: 10.1111/1523-1747.ep12457913.
Acute, low-dose exposure to UVB light reveals a genetic polymorphism in humans with respect to the ability of irradiated skin to support the induction of contact hypersensitivity (CH) to dinitrochlorobenzene (DNCB). In healthy adult caucasians, as well as in humans with deeply pigmented skin, approximately 45% fail to develop CH when DNCB is painted on UVB-irradiated skin; these individuals are termed "UVB susceptible" (UVB-S), whereas those who develop CH at the challenge site are termed "UVB resistant" (UVB-R). The UVB-S trait is characteristic of virtually all patients with biopsy-proved basal/squamous cell cancer, and may therefore be a risk factor for this disease. We have investigated the effects of UVB on expression of primary allergic reactions (PAR) in healthy caucasian and black-skinned adults, as well as patients with skin cancer. Among UVB-R caucasians, very few (less than 25%) developed PAR at site exposed to UVB, whereas among black-skinned UVB-R subjects, all displayed a PAR at the UVB irradiated site. To determine whether the lack of PAR in UVB-R caucasian subjects was systemic or local in origin, DNCB was applied to UVB-exposed buttock skin, and each individual was then challenged with dilute DNCB on forearm skin twice: 11 and 30 d thereafter. When inflammatory responses were evaluated at the original hapten application site, as well as both challenge sites, complete concordance was observed between positive challenge reactions at 30 d (UVB-R) and positive challenge reactions at 11 d, whereas only one caucasian subject displayed a PAR at 12 d. Thus, UVB-R caucasians can display CH as early as 11 d following hapten application to UVB-treated skin, indicating that their failure to display PAR is a local, rather than a systemic, effect of UVB. Because UVB-induced phototoxicity was significantly greater in caucasian than in deeply pigmented skin, it is anticipated that phototoxicity leads to rapid hapten "washout" from UVB-exposed caucasian skin. We propose that PAR usually do not occur in UVB-treated caucasian skin because insufficient hapten remains at the site to trigger a spontaneous inflammation when systemic hapten-specific immunity emerges.
急性低剂量暴露于中波紫外线（UVB）光下，揭示了人类在受照射皮肤支持对二硝基氯苯（DNCB）产生接触性超敏反应（CH）的能力方面存在基因多态性。在健康的成年白种人以及皮肤色素沉着较深的人群中，当在UVB照射过的皮肤上涂抹DNCB时，约45%的人无法产生CH；这些个体被称为“UVB敏感型”（UVB-S），而那些在激发部位产生CH的人则被称为“UVB抵抗型”（UVB-R）。UVB-S特征几乎是所有经活检证实患有基底细胞癌/鳞状细胞癌患者的特点，因此可能是这种疾病的一个风险因素。我们研究了UVB对健康白种人和黑皮肤成年人以及皮肤癌患者原发性过敏反应（PAR）表达的影响。在UVB-R白种人中，很少有人（不到25%）在暴露于UVB的部位出现PAR，而在黑皮肤的UVB-R受试者中，所有人在UVB照射部位都出现了PAR。为了确定UVB-R白种人受试者中PAR的缺乏是全身性的还是局部性的，将DNCB涂抹在暴露于UVB的臀部皮肤上，然后每个个体在前臂皮肤上用稀释的DNCB进行两次激发：分别在11天和30天后。当在最初的半抗原应用部位以及两个激发部位评估炎症反应时，观察到30天（UVB-R）时的阳性激发反应与11天时的阳性激发反应完全一致，而只有一名白种人受试者在12天时出现了PAR。因此，UVB-R白种人在将半抗原应用于UVB处理过的皮肤后11天就可以出现CH，这表明他们未能出现PAR是UVB的局部而非全身性作用。由于UVB诱导的光毒性在白种人中比在色素沉着较深的皮肤中明显更大，预计光毒性会导致半抗原从暴露于UVB的白种人皮肤中迅速“洗脱”。我们提出，在UVB处理过的白种人皮肤中通常不会出现PAR，是因为当全身性半抗原特异性免疫出现时，该部位残留的半抗原不足以引发自发性炎症。
