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Previous Volume 347:55-57 July 4, 2002 Number 1 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The realization that atherosclerosis is, morphologically, an inflammatory disease was originally derived from studies of animal models. Early after the initiation of an atherogenic diet in animals, monocytes adhere to the vascular endothelium and accumulate in lesion-prone arterial sites.¹ This adherence of monocytes to the arterial surface is facilitated by the endothelial expression of surface proteins that are collectively known as adhesion molecules.² Adherent monocytes are enticed into the arterial intima and differentiate into macrophages with the help of such modulators of inflammation as monocyte chemoattractant protein 1 and macrophage colony-stimulating factor, which are produced locally by smooth-muscle cells. Resident . . . [Full Text of this Article]

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