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: 7349298
• 负责人: ROBERT S MITTLER
• 金额: $ 4.01万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-06-09 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7349298
• 关键词: motivation; neoplasm /cancer

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. The goal of this project is to determine how best to utilize CD137 mediated signaling to achieve maximal anti-tumor efficacy and to elucidate the CD137 mediated molecular and biochemical signaling events that drive CD8+ T cells to eradicate tumors that they otherwise fail to respond.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。该项目的目的是确定如何最好地利用CD137介导的信号传导，以达到最大的抗肿瘤功效，并阐明CD137介导的分子和生化信号传导事件，以驱动CD8+ T细胞消除它们否则无法做出反应的肿瘤。