In contrast, natural Tregs expressing CTLA-4, GITR along with high levels of PD-1 tend to release IL-10 and TGF-ß when bound to the PD-L1 expressed by oxidized (ox)-low-density lipoprotein (LDL)-stimulated HUVECs [95], summarizing a possibility for an alternative mechanism by which EC–Treg interactions induce the suppression of inflammation in atherosclerosis. This evidence concerns the gene CD274 and atherosclerosis.