• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose CD1a-DR+ epidermal macrophage induction and Langerhans cell depletion.
【2h】

UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose CD1a-DR+ epidermal macrophage induction and Langerhans cell depletion.

机译：紫外线照射会降低免疫接种率并增强人类对表皮抗原的耐受性：与剂量CD1a-DR +表皮巨噬细胞诱导和朗格汉斯细胞耗竭的关系。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Increasing UVB radiation at the earth's surface might have adverse effects on in vivo immunologic responses in humans. We prospectively randomized subjects to test whether epicutaneous immunization is altered by prior administration of biologically equalized doses of UV radiation. Multiple doses of antigens on upper inner arm skin (UV protected) were used to elicit contact sensitivity responses, which were quantitated by measuring increases in skin thickness. If a dose of UVB sufficient to induce redness (erythemagenic) was administered to the immunization site prior to sensitization with dinitrochlorobenzene (DNCB), we noted a marked reduction in the degree of sensitization (P less than 0.0006) that was highly dose responsive (r = 0.98). Even suberythemagenic UV (less than a visible sunburn) resulted in a decreased frequency of strongly positive responses (32%) as compared to controls (73%) (P = 0.019). The rate of immunologic tolerance to DNCB (active suppression of a subsequent repeat immunization) in the groups that were initially sensitized on skin receiving erythemagenic doses of UV was 31% (P = 0.0003). In addition, a localized moderate sunburn appeared to modulate immunization with diphenylcyclopropenone through a distant, unirradiated site (41% weak responses) as compared to the control group (9%) (P = 0.05). Monitoring antigen presenting cell content in the epidermis revealed that erythemagenic regimens induced CD1a-DR+ macrophages and depleted Langerhans cells. In conclusion, relevant and even subclinical levels of UV exposure have significant down modulatory effects on the ability of humans to generate a T-cell-mediated response to antigens introduced through irradiated skin.
机译：在地球表面增加的UVB辐射可能会对人体的体内免疫反应产生不利影响。我们对受试者进行了前瞻性随机化测试，以测试是否通过事先给予生物学上相等剂量的紫外线辐射来改变表皮免疫。上臂内侧皮肤上的多剂量抗原（受紫外线保护）用于引发接触敏感性反应，通过测量皮肤厚度的增加对其进行定量。如果在用二硝基氯苯（DNCB）致敏之前向免疫部位施用了足以诱导发红的红血球（红肿性），我们注意到对剂量有高度反应的致敏度显着降低（P小于0.0006） = 0.98）。与对照组（73％）相比，即使是红细胞生成的紫外线（少于可见的晒伤）也会导致强阳性反应（32％）的频率降低（P = 0.019）。在最初接受皮肤红斑剂量的紫外线致敏的组中，对DNCB的免疫耐受率（主动抑制后续重复免疫）为31％（P = 0.0003）。此外，与对照组（9％）相比，局部中度晒伤似乎可以通过一个远距离，未辐照的部位（41％较弱的反应）来调节二苯环丙烯酮的免疫接种（P = 0.05）。监测表皮中抗原呈递细胞的含量表明，红斑生成疗法可诱导CD1a-DR +巨噬细胞和耗尽的Langerhans细胞。总之，紫外线暴露的相关甚至亚临床水平对人类对通过辐照皮肤引入的抗原产生T细胞介导的抗原的能力具有显着的向下调节作用。

著录项

相似文献

  • 外文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号