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Monocytes are critical mediators of atherogenesis. Deletion of individual chemokines or chemokine receptors leads to significant but only partial inhibition of lesion development, whereas deficiency in other signals such as CXCL16 or CCR1 accelerates atherosclerosis. Evidence that particular chemokine pathways may cooperate to promote monocyte accumulation into inflamed tissues, particularly atherosclerotic arteries, is still lacking.

circulation

Combined Inhibition of CCL2, CX3CR1, and CCR5 Abrogates Ly6C <sup>hi</sup> and Ly6C <sup>lo</sup> Monocytosis and Almost Abolishes Atherosclerosis in Hypercholesterolemic Mice

Combined Inhibition of CCL2, CX3CR1, and CCR5 Abrogates Ly6C hi and Ly6C lo Monocytosis and Almost Abolishes Atherosclerosis in Hypercholesterolemic Mice

Combined Inhibition of CCL2, CX3CR1, and CCR5 Abrogates Ly6C ^hi and Ly6C ^lo Monocytosis and Almost Abolishes Atherosclerosis in Hypercholesterolemic Mice