Acute coronary syndromes (ACS) are complications of atherosclerotic vascula
r disease that are triggered by the sudden rupture of an atheroma. Atherosc
lerotic plaque stability is determined by multiple factors, of which immune
and inflammatory pathways are critical. Unstable plaque is characterized b
y an infiltrate of T cells and macrophages, thereby resembling a delayed hy
persensitivity reaction. On activation, T cells secrete cytokines that regu
late the activity of macrophages, or the T cells may differentiate into eff
ector cells with tissue-damaging potential. Constitutive stimulation of T c
ells and macrophages in ACS is not limited to the vascular lesion but also
involves peripheral immune cells, suggesting fundamental abnormalities in h
omeostatic mechanisms that control the assembly, turnover, and diversity of
the immune system as a whole. This review gives particular attention to th
e emergence of a specialized T-cell subset, natural killer T cells, in pati
ents with ACS. Natural killer T cells have proinflammatory properties and t
he capability of directly contributing to vascular injury.