Since a link between innate immunity and atherosclerosis has been proposed and several data indicate that signaling through TLR4 promotes atherosclerosis [11], and since HSP60 has been proposed as an endogenous ligand for TLR4 [12], we next evaluated whether HSP60 present in the supernatant of endothelial cells stimulated with anti-US28 antibodies could engage TLR4. Here, TLR4 is linked to atherosclerosis.