Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata.

By C. Swirski, Filip K, Peter Libby, E. Aikawa, P. Alcaide, F. Luscinskas, Ralph Weissleder, M. Pittet, F. Swirski. Journal of Clinical Investigation, 2007

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Immune Effector Mechanisms Implicated in Atherosclerosis: From Mice to Humans (2013, background): “After initiating an atherogenic diet, the blood of hypercholesterolemic mice shows a dramatic increase in Ly6chi monocytes (Swirski et al., 2007) (Tacke et al., 2007).”
Obesity, inflammation, and atherosclerosis (2009, background): “Monocytes seem to commit to distinct roles while in the blood, and exhibit different recruitment mechanisms and functions in the plaque reflected by their surface structure”
Atherosclerosis: current pathogenesis and therapeutic options (2011, background): “In mice, classical Ly6C high cells dominate hyperlipidemia-induced monocytosis and employ the chemokine receptors CCR2, CCR5 and CX3CR1, to invade plaques, where they differentiate into macrophages, whereas entry of patrolling Ly6C low monocytes occurs less frequently and seems to rely on CCR5 (re”
Phenotypic Switching of Adipose Tissue Macrophages With Obesity Is Generated by Spatiotemporal Differences in Macrophage Subtypes (2008, neutral): “This is similar to what has been proposed to mediate monocyte/macrophage recruitment to atherosclerotic plaques (24,25).”