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As the migration of circulating monocytes into the arterial intima and their subsequent differentiation into fat-laden foam cells are critical events in the development of atherosclerosis, the molecular mechanisms underpinning these two events have been the focus of much study in recent years. In particular, since the seminal studies of Goldstein et al. 1 revealed almost 30 years ago that foam cell formation could be triggered by the uptake of oxidized low-density lipoprotein (oxLDL) by macrophage scavenger receptors in vitro , much interest has been focused on the potential of scavenger receptors to modulate atherosclerosis.To date, the class B scavenger receptor CD36 has received the most attention in this context since early studies identified it as a key mediator of oxLDL uptake in vitro .2 However, the results that have emerged from subsequent studies of CD36 function in vivo are both complex and conflicting.3 Febbraio et al. 4,5 were the first to report the results of breeding mice genetically deficient in both CD36 and apolipoprotein E (ApoE), showing that CD36 deficiency reduced aortic lesion formation by ∼76% and that bone-marrow-specific deletion of CD36 also reduced atherosclerosis in ApoE–/– mice. However, the pro-atherogenic potential of CD36 was soon challenged by Freeman and colleagues,6 who reported that genetic deletion of CD36, or the related scavenger receptor SR-A, had no effect on atherosclerosis in their systems and suggested that insufficient … *Corresponding author. Tel: +44 116 256 3048; fax: +44 116 287 5792. E-mail address : ce55{at}le.ac.uk

CD36: promotion from scavenger receptor to mediator of migration?