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Randolph, G. J. Emigration of monocyte-derived cells to lymph nodes during resolution of inflammation and its failure in atherosclerosis. Curr. Opin. Lipidol. 19, 462-468

Department of Gene and Cell Medicine, and the Immunology Institute, 1425 Madison Avenue, Mount Sinai School of Medicine, New York 10029, USA.
Current Opinion in Lipidology (Impact Factor: 5.8). 11/2008; 19(5):462-8. DOI: 10.1097/MOL.0b013e32830d5f09
Source: PubMed

ABSTRACT This review compares the fate of monocyte-derived cells that enter atherosclerotic plaques with those that accumulate at other sites of inflammation.
Resolution of inflammatory reactions involves emigration of monocyte-derived cells out of the inflamed site through nearby lymphatic vessels. However, this emigratory process associated with resolution is impaired in atherosclerosis. The mechanism for impeded emigration from plaques in vivo remains to be determined, but multiple factors are likely involved, including specialized properties of artery walls and a negative impact of lipid mediators on monocyte-derived cell migration.
Impaired egress would be expected to compound macrophage accumulation within plaques, contribute to build-up of necrotic pools, and explain in part the reticence of many plaques to regress, or resolve. Restoration of the capacity of monocyte-derived cells to leave plaques would, by contrast, be expected to facilitate regression, but it remains to be determined whether restoring egress may sometimes provoke unwanted outcomes as well.

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Available from: Gwendalyn J Randolph, May 09, 2014
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    • "This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. EMBO Mol Med (2013) 5, 1901–1917 material, in an atherosclerotic plaque the loading of oxLDL into macrophages shifts them to a more sessile, foam‐cell phenotype, and these foam cells do not leave the lesion after clearing the lipids (Angeli et al, 2004; Randolph, 2008). The trapping of cholesterol‐engorged foam cells causes the plaque to expand through the recruitment of additional leukocytes and vascular smooth muscle cells (VSMCs). "
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