Although injection of IL-33 into apolipoprotein E (ApoE) knockout mice with ongoing atherosclerosis reduced atherosclerotic lesions in thoracic aorta [35], treatment of human endothelial cells with IL-33 increased the expression of adhesion molecules and production of the chemokine monocyte chemoattractant protein (MCP)-1 and promoted adhesion of leukocytes to endothelial cells [36], all of which are features of endothelial activation and are recognized as an early step in the development of atherosclerosis [34]. Here, CCL2 is linked to atherosclerosis.