CCL2 and atherosclerosis: Concluding, inhibition of p55 TNFR remains an attractive candidate for treatment of atherosclerosis since, in addition to our recently described pro-atherosclerotic function of p55 TNFR in regulating foam cell formation and systemic MCP-1 production [10], we here show that this receptor promotes atherosclerosis by inducing endothelial adhesion molecule expression and production of pro-atherosclerotic cytokines and chemokines at the arterial wall.