Beissert S, Hosoi J, Kühn R, Rajewsky K, Müller W, Granstein R D
Massachusetts General Hospital/Harvard Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Boston, USA.
J Invest Dermatol. 1996 Oct;107(4):553-7. doi: 10.1111/1523-1747.ep12582809.
Exposure to mid-range ultraviolet radiation (UVR) [280-320 nm, ultraviolet B (UVB) radiation] inhibits the acquisition of delayed-type hypersensitivity in mice and contact hypersensitivity in rodents and humans. Intraperitoneal administration of interleukin 10 (IL-10) inhibits the sensitization of mice to alloantigens for a delayed-type hypersensitivity reaction and administration of neutralizing antibodies to IL-10 largely, but not totally, blocks the UVR-mediated suppression of the ability to sensitize mice. This suggests that these inhibitory effects of UVB radiation may be mediated by release of IL-10. To test this hypothesis directly, IL-10 gene-targeted (IL-10T) mice lacking expression of IL-10 were examined for the ability of UVB radiation to suppress induction of delayed-type hypersensitivity to alloantigens. IL-10T mice were completely resistant to UVB-induced immunosuppression in this system. Interestingly, UVB radiation could suppress in IL-10T mice the induction of contact hypersensitivity to a hapten applied to the skin at a site distant of irradiation, supporting the concept that regulation pathways of delayed-type hypersensitivity and contact hypersensitivity responses by UVR differ. These data provide additional understanding of the mechanisms of immunosuppression induced by UVR and suggest that IL-10 release subsequent to UVB radiation may play a role in the growth immunogenic UVB-induced cutaneous malignancies in the primary host.
暴露于中波紫外线辐射（UVR）[280 - 320纳米，紫外线B（UVB）辐射]会抑制小鼠迟发型超敏反应的获得以及啮齿动物和人类的接触性超敏反应。腹腔注射白细胞介素10（IL - 10）可抑制小鼠对同种异体抗原的致敏，从而引发迟发型超敏反应，而给予抗IL - 10中和抗体可在很大程度上但并非完全阻断UVR介导的对小鼠致敏能力的抑制。这表明UVB辐射的这些抑制作用可能是由IL - 10的释放介导的。为了直接验证这一假设，研究人员检测了缺乏IL - 10表达的IL - 10基因靶向（IL - 10T）小鼠对UVB辐射抑制同种异体抗原迟发型超敏反应诱导的能力。在该系统中，IL - 10T小鼠对UVB诱导的免疫抑制完全具有抗性。有趣的是，UVB辐射可抑制IL - 10T小鼠对在远离照射部位皮肤涂抹的半抗原的接触性超敏反应诱导，这支持了UVR对迟发型超敏反应和接触性超敏反应调节途径不同的观点。这些数据为UVR诱导免疫抑制的机制提供了更多理解，并表明UVB辐射后IL - 10的释放可能在原发性宿主中UVB诱导的皮肤恶性肿瘤生长免疫原性方面发挥作用。
