Mechanisms underlying the suppression of established immune responses by ultraviolet radiation
Mechanisms underlying the suppression of established immune responses by ultraviolet radiation
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DOI：
10.1046/j.1523-1747.2002.01845.x
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发表时间：
2002-09-01
影响因子：
6.5
通讯作者：
Ullrich, SE
中科院分区：
文献类型：
--
作者：
Nghiem, DX;Kazimi, N;Ullrich, SE
太阳光中的紫外线辐射具有免疫抑制作用。最近，我们表明，太阳模拟紫外线辐射（紫外线A + B; 295-400 nm），应用免疫后，抑制免疫记忆和诱发迟发型超敏反应的常见的机会致病菌，白色念珠菌。此外，我们发现，在太阳光谱的紫外线A区域（320-400 nm）中的波长，没有紫外线B，在激活免疫抑制方面与紫外线A + B辐射同样有效。在这里，我们报告所涉及的机制。免疫后7- 9d暴露于模拟太阳紫外线照射，免疫抑制作用最强。在紫外线照射的小鼠注射抗白细胞介素-10单克隆抗体，或暴露于太阳模拟紫外线照射的小鼠注射重组白细胞介素-12，没有发现免疫抑制。在紫外线A + B照射的小鼠脾脏中发现抑制性淋巴细胞。此外，在紫外线A照射小鼠脾脏中还发现了抗原特异性抑制性T细胞（CD 3（+）、CD 4（+）、DX 5（+））。将含有噬菌体T4 N5的脂质体应用于暴露于太阳模拟紫外线A + B辐射或暴露于紫外线A辐射的小鼠的皮肤，阻断了免疫抑制，证明了紫外线诱导的DNA损伤在抑制已建立的免疫反应中的重要作用。这些发现表明，重叠的免疫抑制机制被紫外线A和紫外线A + B辐射激活。此外，我们的研究结果表明，紫外线辐射激活类似的免疫途径，以抑制诱导或激发免疫反应。
The ultraviolet radiation present in sunlight is immune suppressive. Recently we showed that solar-simulated ultraviolet radiation (ultraviolet A + B; 295-400 nm), applied after immunization, suppressed immunologic memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in the ultraviolet A region of the solar spectrum (320-400 nm), devoid of ultraviolet B, were equally effective in activating immune suppression as ultraviolet A + B radiation. Here we report on the mechanisms involved. Maximal immune suppression was found when mice were exposed to solar-simulated ultraviolet radiation 7-9 d post immunization. No immune suppression was found in ultraviolet-irradiated mice injected with monoclonal anti-interleukin-10 antibody, or mice exposed to solar-simulated ultraviolet radiation and injected with recombinant interleukin-12. Suppressor lymphocytes were found in the spleens of mice exposed to ultraviolet A + B radiation. In addition, antigen-specific suppressor T cells (CD3(+), CD4(+), DX5(+)) were found in the spleens of mice exposed to ultraviolet A radiation. Applying liposomes containing bacteriophage T4N5 to the skin of mice exposed to solar-simulated ultraviolet A + B radiation, or mice exposed to ultraviolet A radiation, blocked immune suppression, demonstrating an essential role for ultraviolet-induced DNA damage in the suppression of established immune reactions. These findings indicate that overlapping immune suppressive mechanisms are activated by ultraviolet A and ultraviolet A + B radiation. Moreover, our findings demonstrate that ultraviolet radiation activates similar immunologic pathways to suppress the induction of, or the elicitation of, the immune response.