Purpose of review: Monocytes play multiple roles in immune system functions and inflammatory diseases such as atherosclerosis. These roles are coupled to diverse trafficking and cellular migration behaviors. Here, we review recent advances in our understanding of such behaviors with emphasis on broad scale trafficking patterns and the cellular and molecular mechanisms regulating diapedesis, a central aspect of trafficking.
Recent findings: Monocytes consist of ‘inflammatory’ and ‘resident’ subsets, which exhibit differential functions and trafficking properties. Notably, the spleen has recently been identified as a reservoir of inflammatory monocytes, which are readily recruited to injured myocardium and possibly other tissues. Resident monocytes have been shown to undergo long-range crawling within the lumen of the microvasculature, which facilitates immune surveillance and rapid response to infection. Monocyte diapedesis has been demonstrated to utilize both para and transcellular migration routes facilitated by endothelial ‘transmigratory cups’. A significant number of new adhesion molecules and signaling pathways have recently been uncovered as functional mediators and modulators of these processes.
Summary: Our improving understanding of monocyte trafficking and migration mechanisms has begun to shed light on the functions of these often enigmatic cells. Continued progress in this area will be critical for elucidating roles of monocytes in disease and for developing therapeutics that target monocytes.
Center for Vascular Biology Research, Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
Correspondence to Christopher V. Carman, PhD, Assistant Professor, Center for Vascular Biology Research, Division of Molecular and Vascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, RN-234, Boston, MA 02215, USA Tel: +1 617 667 0888; fax: +1 617 667 2913; e-mail: email@example.com