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Christian Weber and HIV Infection Killing Two Birds With One Stone : Targeting Chemokine Receptors in Atherosclerosis

The recruitment of mononuclear cells into the arterial wall is a hallmark of atherosclerotic lesion formation. It has been widely acknowledged that the infiltration with monocytes is instrumental in the initiation and progression of atherosclerosis and that this inflammatory process is also driven or sustained by a T helper type 1 (Th1) lymphocyte-mediated immune response.1 Among other proinflammatory cytokines, an abundance of chemokines has been detected in atherosclerotic lesions and has been crucially implicated in directing the recruitment of monocytes and T cells into the lesions.2,3 Notably, genetic deletion or transfer of constructs encoding antagonistic mutants has revealed the essential contribution of certain chemokines and their receptors to lesion formation and macrophage infiltration in atherosclerosis-prone mice, eg, for the prototypic MCP-1 and its receptors CCR2 and for the fractalkine receptor CX3CR.2,3 Moreover, the CCR1 and CCR5 ligand RANTES and the CXCR3 ligands Mig and IP-10 have been found in atherosclerotic lesions. CCR5 and CXCR3 are index chemokine receptors primarily expressed on Th1 T cells guiding their migration to sites of inflammation.4 Although it has become apparent that the involvement of multiple chemokines is more reflective of the robustness and complexity of the recruitment signal required rather than the redundancy of the system, the precise role of these chemokines and their receptors in atherosclerosis has remained elusive until very recently. In addition, it has been questioned whether the involvement of these chemokines corresponds to a specific recruitment of different mononuclear cell types.2,3