Effect of 17β-estradiol on immunosuppression induced by ultraviolet B irradiation
Effect of 17β-estradiol on immunosuppression induced by ultraviolet B irradiation
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DOI：
10.1007/s00403-003-0437-0
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发表时间：
2004-02-01
影响因子：
3
通讯作者：
Inoue, M
中科院分区：
文献类型：
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作者：
Hiramoto, K;Tanaka, H;Inoue, M
背景。女性患皮肤癌的风险低于男性，紫外线（UV）辐射引起的光免疫抑制被认为与皮肤癌的发展有关。目的：观察雌二醇对紫外线B （UVB）照射引起的免疫抑制和接触性超敏反应（CHS）的影响。用0.5%异硫氰酸荧光素（FITC）通过皮肤单次暴露于UVB （10 kJ/m(2)）致敏的C57BL小鼠，可诱导全身免疫抑制。腹腔注射17 -雌二醇、他莫昔芬（17 -雌二醇拮抗剂）或抗雌二醇抗体的小鼠应用FITC后，评估CHS反应。采用酶联免疫吸附试验（ELISA）测定治疗小鼠和对照小鼠血清白介素-10 （IL-10）水平。为了评估17 β -雌二醇对角质形成细胞的影响，我们将Pam-212细胞体外暴露于UVB辐射下，并用17 β -雌二醇处理24小时。采用elisa法测定上清液中IL-10的含量。与未照射小鼠相比，uvb照射小鼠的CHS反应明显受到抑制。连续腹腔注射17β -雌二醇可显著降低uvb诱导的雄性小鼠CHS反应的抑制，而注射他莫昔芬或抗雌二醇抗体可显著促进雌性小鼠uvb诱导的抑制。UVB照射后，17β -雌二醇可降低chs抑制的雄性小鼠的血清IL-10水平，而他莫昔芬或抗雌二醇抗体可提高雌性小鼠的血清IL-10水平。用17 -雌二醇治疗uvb照射的Pam-212细胞，其IL-10的产生呈剂量依赖性。这些结果表明，17 - β -雌二醇可以防止uvb诱导的角化细胞产生的免疫抑制细胞因子引起的CHS反应的抑制。
Background. The risk of skin cancer is lower in females than in males, and photoimmunosuppression caused by ultraviolet (UV) radiation is thought to be involved in the progression of skin cancer.Objectives. To determine the effect of 17beta-estradiol on immunosuppression and contact hypersensitivity (CHS) caused by ultraviolet B (UVB) irradiation.Methods. Systemic immunosuppression was induced in C57BL mice that had been sensitized with 0.5% fluorescein isothiocyanate (FITC) through the skin by a single exposure to UVB (10 kJ/m(2)). The CHS response was assessed after applying FITC to mice treated intraperitoneally with 17beta-estradiol, tamoxifen (17beta-estradiol antagonist), or antiestradiol antibody. Levels of serum interleukin-10 (IL-10) were measured in treated mice and control mice using an enzyme-linked immunosorbent assay (ELISA). To assess the effect of 17beta-estradiol on keratinocytes, Pam-212 cells were exposed in vitro to UVB radiation and treated for 24 h with 17beta-estradiol. The IL-10 content of the supernatant was measured using an ELISA.Results. The CHS response in UVB-irradiated mice was significantly suppressed in comparison to that in nonirradiated mice. Consecutive intraperitoneal injections of 17beta-estradiol significantly reduced UVB-induced suppression of the CHS response in male mice, whereas injection of tamoxifen or antiestradiol antibody significantly promoted UVB-induced suppression in female mice. Treatment with 17beta-estradiol decreased the serum IL-10 levels in CHS-suppressed male mice after UVB irradiation, but treatment with tamoxifen or antiestradiol antibody increased the serum IL-10 levels in female mice. Treatment with 17beta-estradiol reduced IL-10 production by UVB-irradiated Pam-212 cells in a dose-dependent manner.Conclusions. These results suggest that 17beta-estradiol prevents UVB-induced suppression of the CHS response caused by immunosuppressive cytokines produced by keratinocytes.