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Cardiovasc Res. 2015 Aug 1;107(3):321-30. doi: 10.1093/cvr/cvv147. Epub 2015 May 19.

Monocyte trafficking across the vessel wall.

Author information

1
Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, 9420 Athena Cir, La Jolla, CA 92037, USA.
2
Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, 9420 Athena Cir, La Jolla, CA 92037, USA klaus@liai.org.

Abstract

Monocytes fundamentally contribute to immune surveillance and the inflammatory response in immunoinflammatory diseases like atherosclerosis. Recruitment of these cells to the site of injury requires their trafficking across the blood vessel wall. A series of events, including capture, rolling, slow rolling, arrest, adhesion strengthening, and lateral locomotion, precede monocyte transmigration. Recent investigations have revealed new aspects of this cascade. This article revisits some conventional paradigms and selectively highlights new findings, including novel insights into monocyte differentiation and recently identified functional mediators, signalling pathways, and new structural aspects of monocyte extravasation. The emerging roles of endothelial junctional molecules like vascular endothelial-cadherin and the junctional adhesion molecule family, adhesion molecules such as intercellular adhesion molecule-1, molecules localized to the lateral border recycling compartment like cluster of differentiation 99, platelet/endothelial cell adhesion molecule-1, and poliovirus receptor (CD155), as well as other cell surface molecules such as cluster of differentiation 146 and ephrins in transendothelial migration are discussed.

KEYWORDS:

Extravasation; Monocyte migration; Monocyte subsets

PMID:
25990461
PMCID:
PMC4592323
DOI:
10.1093/cvr/cvv147
[Indexed for MEDLINE]
Free PMC Article

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