During the last 2 decades, human and animals studies have clearly documented the crucial role of inflammation in the development and complications of atherosclerosis 1. Both innate and adaptive immunity are involved in this process. The first evidence that suggested a role of adaptive immunity in atherosclerosis was the widespread detection of the major histocompatibility class II in human atherosclerotic plaques, and the presence of a large amounts of CD3+ lymphocytes in human and mouse atherosclerotic lesions. Most of T cells in mouse and human atherosclerotic plaques are CD4+ T-helper (Th) cells expressing the αβ T-cell antigen receptor (TCR). Among CD4+ T cells, Th1 cells have been shown to exert proatherogenic effects, whereas regulatory T cells (Tregs) display atheroprotective properties. The role of Th2 and Th17 cells is still debated