Μελέτη της έκφρασης των υποπληθυσμών των Τ λεμφοκυττάρων σε ασθενείς με έμφραγμα μυοκαρδίου

T cells have been implicated in the pathogenesis of myocardial infarction. Treg alterations in patients with myocardial infarction with ST elevation (STEMI) are not fully elucidated. Platelets from patients with STEMI are activated. How platelets from patients with STEMI interact with other cells is not known. We aimed to investigate whether T cells can be activated by the circulating activated platelets from patients with STEMI and explore how Treg are affected. Methods and Results. Peripheral blood mononuclear cells were isolated from 33 patients with STEMI (29 men, 4 women, mean age 62.5 years) at the time of hospital admission at diagnosis, , as well as 5 days and 30 days later. Ten healthy subjects and 5 patients with unstable angina served as the control and disease-control group, respectively. We analyzed the percentages of CD4+CD25high+FOXP3+ cells representing the regulatory subset (Tregs) at all three time points as described above. The miR155 levels were evaluated using real-time PCR in samples from patients and healthy individuals. T cells that were incubated with platelets from patients with STEMI displayed statistically significant increase of CD69 expression compared to the T cells incubated with platelets from healthy individuals (2.163% vs 0.575%, p =0.013). We then examined the percentages of Treg to explore whether Tregs are altered in order to control the activation that platelets initiate. There was no statistical difference in Treg percentages between patients at presentation and control subjects. However, 5 days later, patients with STEMI displayed a statistically significant increase in Treg numbers compared with the 2 control groups. One month later, Treg numbers returned to the initial presentation levels. Patients with STEMI displayed comparable levels of miR155 at presentation to healthy individuals. Five days later though, patients with STEMI had a statistically significant decrease of miR155 levels (p <0.001) that was inversely correlated with the increased Treg numbers observed at the same time point. Conclusion. We describe for the first time that platelets from patients with STEMI can activate T cells ex vivo, which is specific only for platelets from patients with STEMI. Treg in patients increase shortly after STEMI and return to levels comparable of those of healthy individuals within a month. Mechanistically this up regulation of Treg appeared to be mediated, at least in part, by a decreased expression of miR155. These results suggest that platelets from patients with STEMI can activate the immune system. Tregs increase during the first days after the STEMI and possibly represent the T cell subset that is trying to eliminate the activation of the immune system and the inflammatory response. This observation might lead to the development of novel agents targeting the immune system that could potentially be combined with the current treatment options.