Platelet-Induced T Cell Activation in Patients with Myocardial Infarction; The Role of miR155

Specific aim : We have previously shown that platelets from patients with myocardial infarction (with ST elevation-STEMI) can activate T cells in vitro. In this study we wanted to expand our initial observation and explore the mechanism of this T cell activation. Methods: After written informed consent was obtained, peripheral blood mononuclear cells (PBMCs) were isolated from heparinized venous blood obtained from 30 patients with STEMI (28 men and 2 women) at the time of hospital admission at diagnosis, before receiving any treatment, as well as 5 days and 30 days later. We also analyzed 15 healthy subjects (12 men and 3 women), and 7 patients with unstable angina who served as the disease control group. PBMCs were analyzed by flow cytometry with the following markers and their isotypic controls: CD4, CD25, CD127, FOXP3, and CD69. We also isolated platelet rich plasma or plasma alone from the patients and the healthy subjects, and used in mixed cultures with PBMCs. miR 155 levels were examined with real-time PCR. Results: Initially, we incubated T cells with platelets from patients with STEMI and examined T cell activation by CD69 expression. These T cells showed increased expression of CD69 compared to T cells treated with platelets from healthy subjects (p Next, the percentages of CD4+CD25+hi CD127low FOXP3+ (regulatory T cells, Tregs) were examined in all study subjects. Patients at presentation showed comparable Treg levels with the controls (healthy subjects and disease control group). Five days later, patients with STEMI displayed increased levels of Tregs compared with the controls (p Conclusion : Herein, we show that platelets from patients with STEMI can activate T cells in vitro. This platelet activation in patients with STEMI, results in an increase in Tregs through down-regulation of miR155, that return to normal levels a month later. This Treg increase reflects possibly an effort to suppress immune system activation secondary to platelet activation, shortly after the infarct. Disclosures No relevant conflicts of interest to declare.