CD69 expression in regulatory T cells protects from the immune-mediated damage after myocardial infarction

Abstract CD69 depletion from the lymphoid compartment promotes a Th17/Treg imbalance and exacerbates development of atherosclerosis. As atherosclerosis is trigger myocardial infarction, we have analyzed role in Treg cells after a) permanent occlusion left-anterior-descending coronary artery (LAD-ligation) mice, b) angiography two cohorts acute infarction (MI) patients. Our data show that expression critical to maintain immune homeostasis increases overall survival mice LAD-ligation. Cd69−/− develop IL17A+ gdT cell responses early ischemia increment inflammation and, consequently, worsen cardiac function. Furthermore, found CD69+ induce apoptosis diminish IL-17A production by mechanism dependent on membrane CD39 ectonucleotidase activity. The adoptive transfer LAD-ligation reduces recruitment, resulting increased improved outcome. In accordance, independent patients indicate levels blood MI associated with lower risk developing chronic heart failure. support prevent excess damage MI, whose value remains function medium term. Funding Acknowledgement Type funding sources: Public grant(s) – National budget only. Main source(s): Fondo de Investigaciones Sanitarias. Instituto Salud Carlos III. Ministerio Ciencia Innovaciόn y Universidades (Spanish Government). Summary immage