Chung H T, Burnham D K, Robertson B, Roberts L K, Daynes R A
J Immunol. 1986 Oct 15;137(8):2478-84.
Our study was designed to analyze the possible involvement of prostaglandins in the mechanisms responsible for the depressions in contact hypersensitivity (CH) responsiveness observed in UVR-exposed animals. Low-dose UVR-exposed animals were found to exhibit a depressed capacity to elicit CH responses after hapten application to irradiated (devoid of Langerhans cells) or UVR-protected (normal Langerhans cells) dorsal skin surfaces. Normal responsiveness was observed in low-dose UVR-exposed animals sensitized through unirradiated ventral skin surfaces. Indomethacin treatment of low-dose UVR-exposed animals (to inhibit prostaglandin synthesis in vivo) caused a retention in the capacity to respond normally to CH induction to haptens applied to the nonirradiated, but not to irradiated, dorsal skin surfaces. High-dose UVR-exposed animals, which normally exhibit a depression in responsiveness to hapten sensitization, retained a normal capacity to elicit CH responses if treated with the drug indomethacin. These findings implicate prostaglandins in the pathogenesis of the immunologic hyporesponsiveness, observed in low- and high-dose UVR-exposed animals. Our studies also determined that under all experimental conditions where animals were contact sensitized through nonirradiated skin sites, CH-effector cells could be found in the draining lymph nodes. No CH-effector cells were observed in the lymph nodes of mice that were contact sensitized directly through irradiated skin sites. It was also found that the spleens of both UVR-exposed and normal animals contained adoptively transferrable suppressor cells subsequent to hapten application. This demonstration of CH-effector and CH-suppressor cells in both normal and UVR-exposed animals did not directly relate to the potential of the donor animals to elicit a CH response.
我们的研究旨在分析前列腺素是否可能参与了紫外线照射动物中观察到的接触性超敏反应（CH）反应性降低的机制。发现低剂量紫外线照射的动物在将半抗原应用于照射过的（无朗格汉斯细胞）或紫外线防护的（正常朗格汉斯细胞）背部皮肤表面后，引发CH反应的能力降低。通过未照射的腹部皮肤表面致敏的低剂量紫外线照射动物表现出正常反应性。用吲哚美辛处理低剂量紫外线照射的动物（以抑制体内前列腺素合成），导致对应用于未照射但非照射的背部皮肤表面的半抗原诱导的CH反应正常反应能力得以保留。高剂量紫外线照射的动物通常对半抗原致敏反应性降低，但如果用吲哚美辛治疗，则保留了引发CH反应的正常能力。这些发现表明前列腺素参与了在低剂量和高剂量紫外线照射动物中观察到的免疫低反应性的发病机制。我们的研究还确定，在所有通过未照射皮肤部位进行接触致敏的实验条件下，在引流淋巴结中均可发现CH效应细胞。在通过照射皮肤部位直接进行接触致敏的小鼠淋巴结中未观察到CH效应细胞。还发现，在应用半抗原后，紫外线照射动物和正常动物的脾脏中均含有可过继转移的抑制细胞。在正常动物和紫外线照射动物中CH效应细胞和CH抑制细胞的这种表现与供体动物引发CH反应的潜力没有直接关系。
