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。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。该项目的目标是确定如何最好地利用CD 137介导的信号传导来实现最大的抗肿瘤功效，并阐明CD 137介导的分子和生化信号传导事件，这些事件驱动CD 8 + T细胞根除肿瘤，否则它们无法响应。