LDLR and atherosclerosis: We and others have shown previously that the majority of T-cells in an atherosclerotic lesion are CD4+ T-helper type 1 cells that produce interferon-γ2–12 and deficiency in either interferon-γ or the transcription factor T-bet (required for T-helper type 1 differentiation) attenuates the progression of atherosclerosis in cholesterol-fed low-density lipoprotein receptor null mice (Ldlr−/−).