Role of autophagy in T regulatory cells-polarization during atherosclerotic disease

Atherosclerosis is a chronic inflammatory disorder of the large arteries and represents the primary cause of heart disease and stroke. The exact cause of atherosclerosis is not known. A variety of studies show that autophagy deficiency may be pro-atherogenic and the role of autophagy in smooth muscle cells, macrophages and endothelial cells has been investigated[1]. However, to date no studies addressed the effect of autophagy on leukocyte subsets playing a role in plaque formation and development. The presentproject aims to better clarify the role played by autophagy in lymphocyte homeostasis in human atherosclerotic plaques and in APOE-KO, a mouse model of atherogenesis[2]. In particular, we will investigate cell-autonomous autophagy in mouse Tconv/Tregfunctions, evaluate autophagy-driven T cell polarization in stabilizing atherosclerotic plaques in a mouse model mouse of atherosclerosis. The comprehension of the role of autophagy as a further mechanism underlying Treg induction and stability may open new therapeutic avenues for atherosclerosis.