B 26 - Regulation of T cell plasticity and metabolism by coagulation regulators

Within the 2nd funding period, project B 26 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 A 05, Z 01). Within the 3rd funding period we will investigate specific candidate receptors (e.g. integrins, S1PR1, cooperation with A 20, B 12), the metabolic signature, and signaling pathways (cooperation with A 04, A 23, B 14, B 16, B 19). 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.