Fig 2: Expression level of the P2RY11 gene was analyzed by RT-qPCR (A) and P2Y11 protein expression by flow cytometry (MFI) in CD3 + cells (B,E), CD19 + cells (C,f) and CD11c + CD14 + cells (D). RT-qPCR: n = 17 samples in healthy donors, n = 40 samples in H0-H48 group, n = 37 in D3 group, n = 10 in M1 group, n = 95 in M6-M12 group; flow cytometry: n = 4 samples in healthy donors group, n = 34 to 40 samples in H0-H48 group, n = 5 to 8 samples in M1 group. *p < 0.05, ****p < 0.001.

Fig 3: Acute myocardial infarction (AMI) is responsible for an increase of P2Y11 expression in PBMC that could lead to a modification of immune cells transcriptional profile resulting in a tolerogenic polarization of dendritic cells and a decrease of Th1/Th2 ratio. P2Y11 receptor could also be involved in PBMC hyporesponsiveness early after AMI and, as a consequence in cytokines and chemokines secretion changes. This immune peripheral response may partly explain the tissue response including differenciation of fibroblasts in myofibroblasts. P2Y11 represents a cornerstone of the control of inflammatory response after myocardial infarction.