CD137 SIGNALS IN DC DURING AG-PRIMING INDUCES TOLERANCE

AG 启动期间 DC 中的 CD137 信号会导致容差

• 批准号: 7715769
• 负责人: ROBERT S MITTLER
• 金额: $ 3.56万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715769
• 关键词: Acute; CD8B1 gene; Computer Retrieval of Information on Scientific Projects Database; Dendritic Cells; Funding; Grant; Infection; Influenza; Institution; Lymphocytic choriomeningitis virus; Mediating; Mus; Reporting; Research; Research Personnel; Resources; Signal Transduction; Source; T-Lymphocyte; Transgenic Organisms; United States National Institutes of Health; cell type

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In the previous reporting period we confirmed that anti-CD137-mediated suppression could be induced in CD8 T cells, as well as CD4 T. Using P14 TCR transgenic T cells and CD137-deficient mice and we had found that the induction of suppression caused by anti-CD137 was independent of CD137 expression on T cells, and that the targeted cell type might be a subset of dendritic cells. In this reporting period we revisited the question of how anti-CD137 mAb signaling induced suppression of both CD4 and CD8 T cells during an acute LCMV Armstrong infection and in an acute influenza infection.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 中心，不一定是研究者的机构。 在之前的报告期中，我们证实抗CD137介导的抑制可以在CD8 T细胞以及CD4 T细胞中诱导。使用P14 TCR转基因T细胞和CD137缺陷小鼠，我们发现由以下因素引起的抑制的诱导抗 CD137 独立于 T 细胞上的 CD137 表达，并且目标细胞类型可能是树突状细胞的子集。 在本报告期内，我们重新讨论了抗 CD137 mAb 信号传导如何在急性 LCMV 阿姆斯特朗感染和急性流感感染期间诱导 CD4 和 CD8 T 细胞抑制的问题。