In a mouse model of atherosclerosis, depletion of pDCs using multiple antibodies against bone marrow stromal cell antigen 2 (BST2) promotes the accumulation of T cells in plaques, leading to enhanced atherosclerosis in Ldlr-/- mice (168); whereas in ApoE-/- mice, atherosclerosis is reduced by decreasing macrophage infiltration in plaques and stabilizing plaques by increasing collagen content (169, 170). This evidence concerns the gene APOE and atherosclerosis.