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Review
. 2011 Dec;3(12):713-25.
doi: 10.1002/emmm.201100183. Epub 2011 Oct 28.

Chemokines: established and novel targets in atherosclerosis

Rory R Koenen  1 , Christian Weber
Affiliations
Review

Chemokines: established and novel targets in atherosclerosis

Rory R Koenen et al. EMBO Mol Med. 2011 Dec.

Abstract

In their role as small chemotactic cytokines, chemokines are crucial mediators and regulators of leukocyte trafficking during immune surveillance and inflammation. Their involvement in the development and progression of inflammatory diseases has been subject of intense investigation. Concordantly, the chemokine system has been explored in search for therapeutic targets to prevent or treat inflammatory disorders, such as atherosclerosis. Targeting the chemokine system offers various entry points for a causative treatment of this widespread and chronic illness. Although this approach has encountered some setbacks, several innovative compounds are currently in an advanced stage of development. In this review, the current standing of this dynamic field is highlighted and the potential advantages and drawbacks of particular strategies are discussed.

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Figures

Figure 1
Figure 1. Schematic representation of novel chemokine players in atherosclerosis and their mechanism of action towards their target cells
Neutrophils and Ly6Chi monocytes emigrate from the bone marrow through action of chemokines CXCL12 or CCL2/-20, respectively, and are recruited to atherosclerotic plaques by chemokines (e.g. CXCL1 or CX3CL1) presented on endothelial cells of the inflamed vessel wall. Inside the plaque, the CX3CL1–CX3CR1 axis promotes Ly6Chi monocyte survival. Dendritic cells expressing CCL17 may control the expansion of Treg in plaques and lymph nodes. Migration to and from lymphoid organs, as well as T cell priming are mediated by signalling between CCL19/-21 and CCR7 on T cells and dendritic cells.
See this image and copyright information in PMC

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