...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Regulation Of Cytotoxic T Lymphocyte Triggering By Pir-b On Dendritic Cells
【24h】

Regulation Of Cytotoxic T Lymphocyte Triggering By Pir-b On Dendritic Cells

机译：Pir-b触发树突状细胞对细胞毒性T淋巴细胞的调节

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Priming of cytotoxic T lymphocytes (CTLs) by dendritic cells (DCs) is crucial for elimination of pathogens and malignant cells. To activate CTLs, DCs present antigenic peptide-complexed MHC class I molecules (MHC-I) that will be recognized by the CTLs with T cell receptors and CD8 molecules. Here we show that paired Ig-like receptor (PIR)-B, an MHC-I receptor expressed on antigen-presenting cells, can regulate CTL triggering by blocking the access of CD8 molecules to MHC-I. PIR-B-deficient DCs evoked CTLs more efficiently, leading to accelerated graft and tumor rejection. PIR-B~+ non-DC transfectant cells served as less efficient stimulators and targets for CTLs than PIR-B~-cells at the effector phase in vitro. On surface plasmon resonance analysis, PIR-B and CD8αα were revealed to compete in binding to MHC-I. Our results may provide a novel strategy for regulating CTL-mediated immunity and diseases in a sterical manner.
机译：树突状细胞（DC）引发细胞毒性T淋巴细胞（CTL）对于消除病原体和恶性细胞至关重要。为了激活CTL，DC会呈递抗原肽复合MHC I类分子（MHC-1），CTL会通过T细胞受体和CD8分子识别这些分子。在这里，我们显示成对的Ig样受体（PIR）-B（在抗原呈递细胞上表达的MHC-1受体）可以通过阻止CD8分子进入MHC-1来调节CTL触发。缺乏PIR-B的DC更有效地诱发CTL，从而导致移植物和肿瘤排斥反应加速。在体外，在效应子阶段，PIR-B〜+非DC转染细胞比CIR-B〜-细胞更不适合作为CTL的刺激物和靶标。在表面等离振子共振分析上，PIR-B和CD8αα显示出与MHC-1的结合竞争。我们的结果可能为以空间方式调节CTL介导的免疫和疾病提供了一种新的策略。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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