Reeve V E, Boehm-Wilcox C, Bosnic M, Cope R, Ley R D
Department of Veterinary Pathology, University of Sydney, NSW, Australia.
Photochem Photobiol. 1994 Sep;60(3):268-73. doi: 10.1111/j.1751-1097.1994.tb05103.x.
The immunological consequences of exposure to UVA (320-400 nm) radiation are unclear. This study describes the relationship between the generation of epidermal cis-urocanic acid and the ability to respond to a contact-sensitizing agent, in hairless mice exposed to different UV radiation sources, which incorporate successively greater short-wavelength cutoff by filtration of the radiation from fluorescent UV tubes. Mice were exposed to these radiation sources at doses systematically varying in UVB radiation content but supplying increasing proportions of UVA radiation. All radiation sources were found to generate approximately 35% cis-urocanic acid in the epidermis, thus normalizing the sources for cis-urocanic acid production. However, only those sources richest in short-wavelength UVB resulted in suppression of the systemic contact hypersensitivity response. These sources also induced the greatest erythema reaction, measured as its edema component, in the exposed skin. A strong correlation was thus demonstrated between the induction of edema and the suppression of contact hypersensitivity, but there appeared to be no correlation between the generation of epidermal cis-urocanic acid and suppression of contact hypersensitivity. The sources richest in UVA content did not result in suppression of contact hypersensitivity; furthermore mice previously irradiated with such UVA-rich sources were refractory to the immunosuppressive action of exogenous cis-urocanic acid. A protective effect of the increased UVA content thus appeared to be inhibiting immunosuppression by the available endogenously generated or exogenously applied cis-urocanic acid.
暴露于UVA（320 - 400纳米）辐射后的免疫学后果尚不清楚。本研究描述了在无毛小鼠中，暴露于不同紫外线辐射源后，表皮顺式尿刊酸的生成与对接触致敏剂的反应能力之间的关系。这些辐射源通过过滤来自荧光紫外线灯管的辐射，依次具有更短的短波截止波长。小鼠以系统变化的UVB辐射含量但UVA辐射比例增加的剂量暴露于这些辐射源。发现所有辐射源在表皮中产生约35%的顺式尿刊酸，从而使顺式尿刊酸生成的来源标准化。然而，只有那些富含短波UVB的辐射源导致全身接触超敏反应受到抑制。这些辐射源在暴露皮肤中也引起最大的红斑反应，以其水肿成分来衡量。因此，水肿的诱导与接触超敏反应的抑制之间表现出强烈的相关性，但表皮顺式尿刊酸的生成与接触超敏反应的抑制之间似乎没有相关性。富含UVA的辐射源不会导致接触超敏反应受到抑制；此外，先前用此类富含UVA的辐射源照射过的小鼠对外源性顺式尿刊酸的免疫抑制作用具有抗性。因此，增加的UVA含量似乎具有保护作用，可抑制内源性生成或外源性应用的顺式尿刊酸的免疫抑制作用。
