• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >B7-H1 on myeloid-derived suppressor cells in immune suppression by a mouse model of ovarian cancer.
【24h】

B7-H1 on myeloid-derived suppressor cells in immune suppression by a mouse model of ovarian cancer.

机译：B7-H1对骨髓来源的抑制细胞的卵巢癌小鼠模型具有免疫抑制作用。

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

Myeloid-derived suppressor cells (MDSCs) accumulate in tumor-bearing hosts and are associated with immune suppression. Here, we described high level of expression of B7-H1 (CD274), PD-1 (CD279) and CTLA4 (CD152) by Gr-1(+)CD11b(+) MDSCs obtained from both ascites and spleens of mice bearing the 1D8 ovarian carcinoma, whereas B7-DC (CD273), CD40 and CD86 were absent. In contrast, B7-H1, PD-1 and CTLA-4 expression was not detected on Gr-1(+)CD11b(+) cells from naive mice. Expression of B7-H1 by Gr-1(+)CD11b(+) cells from naive mice could be induced by co-culture with 1D8 ovarian carcinoma cells. Gr-1(+)CD11b(+) cells derived from 1D8 tumor-bearing mice markedly suppressed antigen-specific immune responses, whereas Gr-1(+)CD11b(+) cells from naive mice did not. siRNA-mediated knockdown of B7-H1 in Gr-1(+)CD11b(+) cells of 1D8 tumor-bearing mice alleviated suppression of antigen-specific immune responses. Suppression of antigen-specific immune responses via B7-H1 on Gr-1(+)CD11b(+) myeloid cells was mediated by CD4(+)CD25(+) Foxp3(+) T regulatory cells and required PD-1. Antibody blockade of either B7-H1 or PD-1 retarded the growth of 1D8 tumor in mice. This suggests that expression of B7-H1 on Gr-1(+)CD11b(+) myeloid cells triggered by the 1D8 mouse model of ovarian carcinoma suppresses antigen-specific immunity via interaction with PD-1 on CD4(+)CD25(+) Foxp3(+) regulatory T cells.
机译：髓样来源的抑制细胞（MDSC）积累在荷瘤宿主中，并与免疫抑制相关。在这里，我们描述了通过从带有1D8小鼠的腹水和脾脏中获得的Gr-1（+）CD11b（+）MDSCs高水平表达B7-H1（CD274），PD-1（CD279）和CTLA4（CD152）卵巢癌，而没有B7-DC（CD273），CD40和CD86。相比之下，未从原始小鼠的Gr-1（+）CD11b（+）细胞上检测到B7-H1，PD-1和CTLA-4的表达。通过与1D8卵巢癌细胞共培养可以诱导来自天真小鼠的Gr-1（+）CD11b（+）细胞表达B7-H1。来自1D8荷瘤小鼠的Gr-1（+）CD11b（+）细胞显着抑制了抗原特异性免疫反应，而来自未加工小鼠的Gr-1（+）CD11b（+）细胞却没有。 siRNA介导的1D8荷瘤小鼠Gr-1（+）CD11b（+）细胞中B7-H1的敲低减轻了抗原特异性免疫反应的抑制。通过CD7（+）CD25（+）Foxp3（+）T调节细胞和所需的PD-1介导通过B7-H1对Gr-1（+）CD11b（+）髓样细胞的抗原特异性免疫反应的抑制。 B7-H1或PD-1的抗体阻滞可延缓小鼠1D8肿瘤的生长。这表明卵巢癌的1D8小鼠模型触发的Gr-1（+）CD11b（+）髓样细胞上B7-H1的表达通过与CD4（+）CD25（+）上的PD-1相互作用抑制抗原特异性免疫。 Foxp3（+）调节性T细胞。

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