[Atherosclerosis : on the trail of chemokines]

Atherosclerosis, which is more than a problem of lipid metabolism, is associated with chronic inflammation of large arteries. This is notably caused by the recruitment of circulating blood monocytes to the arterial wall. Extensive studies in humans and mice have shown that the chemokines and their receptors, responsible for leukocyte recirculation, are strongly implicated in the initial onset of atherosclerosis. Murine models have provided further proof of the role of the CCR2/CCL2, CX3CR1/CXCL16 and CCR5/CCL5 axes in the different stages of disease, as well as the preventative roles of CCR1/CCL5 and CXCR6/CXCL16. The integration at the cellular level of various signals in the chemokine network underlines the complex process of leukocyte recruitment to the lesional area. Furthermore the capacity of chemokines to modulate atherosclerosis lies not just with their chemoattractant properties but also with their influence on leukocyte homeostasis. These molecules have therefore quickly become therapeutic targets for atherosclerosis and have opened up new avenues for treating inflammatory diseases. This review principally addresses the implication of chemokines and their receptors in the initial recruitment steps of blood monocytes, and provides an overview of recent research on these molecular controllers of inflammation.