Regulation of T cell plasticity and metabolism by coagulation regulators (B26)

凝血调节剂对 T 细胞可塑性和代谢的调节 (B26)

• 批准号: 251753274
• 金额: --
• 依托单位: Institut für Laboratoriumsmedizin, Klinische Chemie und Molekulare Diagnostik
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2014
• 资助国家: 德国
• 起止时间: 2013-12-31 至 2020-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/251753274?language=en
• 关键词: Regulation; cell; plasticity; metabolism; coagulation

Within the 2nd funding period, project B26 established that coagulation protease activated protein C (aPC) acts directly on primary T cells via the receptor-heterodimer PAR2/PAR3, promoting expansion of Tregs and protecting from GvHD (graft versus host disease; cooperation with A05, Z01). Within the 3rd funding period we will investigate specific candidate receptors (e.g. integrins, S1PR1, cooperation with A20, B12), the metabolic signature, and signaling pathways (cooperation with A04, A23, B14, B16, B19). Furthermore, the relevance of platelets for the coagulation protease aPC-dependent effect on T cells will be investigated, focusing on mechanistic studies related to platelet-derived extracellular vesicles, ATP/ADP and potentially involved receptors.

在第二个资助期内，B26项目确定凝血蛋白酶活化蛋白C （aPC）通过受体异源二聚体PAR2/PAR3直接作用于原代T细胞，促进treg扩增，保护GvHD（移植物抗宿主病；与A05， Z01合作）。在第三个资助期内，我们将研究特定的候选受体（如整合素，S1PR1，与A20， B12合作），代谢特征和信号通路（与A04， A23, B14, B16， B19合作）。此外，将研究血小板与凝血蛋白酶apc依赖性作用对T细胞的相关性，重点研究血小板来源的细胞外囊泡、ATP/ADP和可能涉及的受体的机制。