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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 在上一个报告期间，我们证实了抗CD 137介导的抑制可以在CD 8 T细胞以及CD 4 T细胞中诱导。利用P14 TCR转基因T细胞和CD 137缺陷小鼠，我们发现抗CD 137引起的抑制的诱导与T细胞上的CD 137表达无关，并且靶细胞类型可能是树突状细胞的一个亚群。 在本报告期内，我们重新讨论了抗CD 137 mAb信号传导如何在急性LCMV Armstrong感染和急性流感感染期间诱导CD 4和CD 8 T细胞抑制的问题。