Summary
Chemokines play an important role in inducing chemotaxis of cells, piloting white
blood cells in immune surveillance and are crucial parts in the development and progression
of atherosclerosis. Platelets are mandatory players in the initiation of atherosclerotic
lesion formation and are susceptible targets for and producers of chemokines. Several
chemokine receptors on platelets have been described previously, amongst them CX3CR1, the receptor for fractalkine. The unique chemokine fractalkine (CX3CL1, FKN) exists as a soluble as well as a membrane-anchored glycoprotein. Its essential
role in the formation of atherosclerotic lesions and atherosclerosis progression has
been impressively described in mouse models. Moreover, fractalkine induces platelet
activation and adhesion via a functional fractalkine receptor (CX3CR1) expressed on the platelet surface. Platelet activation via the FKN/CX3CR1-axis triggers leukocyte adhesion to activated endothelium, and fractalkine-induced
platelet P-selectin is mandatory for leukocyte recruitment under arterial flow conditions.
This review summarises the role of fractalkine as a potential local inflammatory mediator
which influences platelet activation in the setting of atherosclerosis. Beyond that,
aspects of a potential interaction between fractalkine and platelet responsiveness
to antiplatelet drugs are described. Furthermore, the possible impact of high-density
lipoprotein cholesterol (HDL-C) on atherosclerosis progression, platelet activation
and fractalkine signalling are discussed.
Keywords
Fractalkine - platelet activation - atherosclerosis - HDL