Ullrich Stephen E, Kripke Margaret L, Ananthaswamy Honnavara N
Department of Immunology, University of Texas M. D. Anderson Cancer Center, Texas Medical Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Exp Dermatol. 2002;11 Suppl 1:13-6. doi: 10.1034/j.1600-0625.11.s.1.4.x.
The ultraviolet (UV) radiation present in sunlight is immune-suppressive. Recently we showed that solar-simulated UV radiation (UVA + UVB; 295-400 nm), applied after immunization, suppressed immunological memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in the UVA region of the solar spectrum (320-400 nm), devoid of UVB, were equally effective in activating immune suppression as UVA + UVB radiation. Here we report on the mechanisms involved. No immune suppression was found in UV-irradiated mice injected with monoclonal anti-interleukin (IL)-10 antibody, or mice exposed to solar-simulated UV radiation and injected with recombinant IL-12. Antigen-specific suppressor T cells were found in the spleens of mice exposed to UVA + UVB radiation. Applying liposomes containing bacteriophage T4N5 to the skin of mice exposed to solar-simulated UVA + UVB radiation or mice exposed to UVA radiation blocked immune suppression, demonstrating an essential role for UV-induced DNA damage in the suppression of established immune reactions. These findings indicate that UV radiation activates similar immunological pathways to suppress the induction, or the elicitation, of the immune response.
阳光中存在的紫外线（UV）具有免疫抑制作用。最近我们发现，免疫接种后施加的模拟太阳紫外线辐射（UVA + UVB；295 - 400纳米）会抑制免疫记忆以及对常见机会性病原体白色念珠菌的迟发型超敏反应的激发。此外，我们发现太阳光谱UVA区域（320 - 400纳米）中不含UVB的波长，在激活免疫抑制方面与UVA + UVB辐射同样有效。在此我们报告其中涉及的机制。在注射了单克隆抗白细胞介素（IL）-10抗体的紫外线照射小鼠中，或在暴露于模拟太阳紫外线辐射并注射了重组IL-12的小鼠中，均未发现免疫抑制现象。在暴露于UVA + UVB辐射的小鼠脾脏中发现了抗原特异性抑制性T细胞。将含有噬菌体T4N5的脂质体应用于暴露于模拟太阳UVA + UVB辐射的小鼠皮肤或暴露于UVA辐射的小鼠皮肤，可阻断免疫抑制，这表明紫外线诱导的DNA损伤在抑制已建立的免疫反应中起重要作用。这些发现表明，紫外线辐射激活了类似的免疫途径来抑制免疫反应的诱导或激发。
