Hapten-specific tolerance induced by acute, low-dose ultraviolet B radiation of skin is mediated via interleukin-10.
Hapten-specific tolerance induced by acute, low-dose ultraviolet B radiation of skin is mediated via interleukin-10.
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由皮肤的急性、低剂量紫外线 B 辐射诱导的半抗原特异性耐受是通过白细胞介素 10 介导的。
DOI：
10.1111/1523-1747.ep12276415
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Streilein,JW
中科院分区：
文献类型：
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作者：
Niizeki,H;Streilein,JW
由于白细胞介素(IL)-10是一种免疫调节细胞因子，由暴露于UVB辐射（UVR）的角质形成细胞产生，我们确定了IL-10是否参与急性低剂量UVR后失败的接触超敏反应（CH）诱导或耐受。小鼠重组IL-10 （200 ng）皮下注射于刮除的腹部皮肤。为了评估IL-10对CH诱导的影响，在注射IL-10后30 min内将185μg的二硝基氟苯（DNFB）涂在皮肤上，5 d后用稀释的DNFB攻耳检测。为了评估耐受性，在il -10注射皮肤上第一次涂DNFB （185μg）后14 d，在正常体壁皮肤上第二次涂DNFB (185μg)；第19天测定CH。我们发现，在注射il -10的皮肤上接受DNFB的小鼠产生的CH的强度与注射pbs的对照组相当。因此，如果在30分钟内将半抗原涂在注射部位，则该剂量的IL-10不会对CH诱导产生有害影响。相比之下，在皮下注射IL-10后30分钟、1天或3天内首次经历DNFB的小鼠表现出半抗原特异性耐受性。此外，腹腔注射抗il -10抗体可阻止UVR-和顺式尿酸依赖性耐受；抗il -10抗体对TNF-α-诱导的耐受性无影响，UVR暴露后不能恢复CH诱导。这些数据表明，IL-10是暴露于急性低剂量紫外线照射的动物皮肤上半抗原诱导耐受的重要介质。
Because interleukin (IL)-10 is an immunoregulatory cytokine that is produced by keratinocytes exposed to UVB radiation (UVR), we determined whether IL-10 participates in either failed contact hypersensitivity (CH) induction or tolerance after acute, low-dose UVR. Murine recombinant IL-10 (200 ng) was injected intradermally on shaved abdominal skin. To assess the effects of IL-10 on CH induction, dinitrofluorobenzene (DNFB, 185μg) was painted on the skin within 30 min after IL-10 was injected, and the mice were assayed 5 d later by ear challenge with dilute DNFB. To assess tolerance, DNFB (185μg) was painted a second time on normal body-wall skin 14 d after DNFB was first painted on IL-10-injected skin; CH was then assayed on day 19. We found that mice that received DNFB on IL-10-injected skin developed CH comparable in intensity to that observed in PBS-injected controls. Thus, this dose of IL-10 did not prove to be deleterious to CH induction if hapten was painted on the injected site within 30 min. By contrast, mice that first experienced DNFB within 30 min, 1 d, or 3 d after IL-10 had been injected intracutaneously displayed hapten-specific tolerance. Moreover, intraperitoneally injected anti-IL-10 antibody prevented UVR- and cis-urocanic acid-dependent tolerance; anti-IL-10 antibody had no effect on TNF-α-induced tolerance and failed to restore CH induction after UVR exposures. These data indicate that IL-10 is an important mediator of the tolerance induced when hapten is painted on the skin of animals exposed to acute, low-dose UVR.