The CD73-adenosine-Interleukin 6-type cytokines axis in myocardial infarction (B01[02])

该提案基于Schrader实验室（嘌呤能信号传导）和舍勒实验室（白细胞介素（IL-）6-生物学）的互补专业知识，并建立在前一个资助期获得的关于CD 73衍生腺苷和A2 B受体介导的IL-6产生相互作用的结果基础上。我们认为心肌细胞和非心肌细胞（心外膜衍生细胞、成纤维细胞、免疫细胞）是各种促炎细胞因子（如IL-6）的重要来源，这些细胞因子由T细胞CD 73衍生的腺苷控制，从而形成MI后心脏的整体免疫反应。

This proposal is based on the complementary expertise of the Schrader Lab (purinergic signaling) and the Scheller lab (Interleukin (IL-)6-biology) and builds on results obtained in the previous funding period on the interplay of CD73-derived adenosine and A2B-receptor-mediated IL-6 production. We propose that cardiomyocytes and non-cardiomyocytes (epicardial derived cells, fibroblasts, immune cells) are important sources of various pro-inflammatory cytokines such as IL-6 that are controlled by T-cell CD73-derived adenosine, which shapes the overall immune response in the post-MI heart.