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

这项建议基于Schrader Lab(嘌呤能信号传递)和Scheller Lab(白介素6-生物学)的互补专业知识，并建立在上一个资助期关于CD73衍生的腺苷和A2B受体介导的IL-6产生的相互作用的结果的基础上。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的重要来源，如IL-6，这些细胞因子由T细胞CD73衍生的腺苷控制，形成心肌梗死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.