During the last two decades, a new perspective on atherosclerosis has prevailed based on accumulating evidence on the role of inflammatory and immune-competent cells, such as monocytes and T-lymphocytes, in contributing to the development of this disease. It is now generally accepted that a specific T-cell response is crucial in determining not only the development and growth of the atherosclerotic lesion, but also its fate toward a stable or an unstable pattern of evolution (i.e., rupture or ulceration), eventually leading to the clinical occurrence of acute coronary syndromes (ACS) [1]. In this respect, a complex interplay between T-cell subsets seems to regulate the fate of atherosclerotic lesions [2]. The adaptive effector CD4+ T helper (Th)-mediated immune response can be very heterogeneous, because of the existence of distinct cell subsets characterized by different profiles of cytokine production. Two polarized types of Th effectors, type 1 (Th-1) and type 2 (Th-2), were initially identified in bothmice and humans. Th-1 cells produce large amounts of interferon (IFN)-γ, while Th-2 cells are characterized by the production of IL-4, IL-5, and IL-13, but not IFN-γ. Our group has previously shown that Th-1 cells, by producing large amounts of γ-IFN, may contribute to