| Literature DB >> 27668800 |
Mark Roufaiel1,2, Eric Gracey3,4, Allan Siu1,2, Su-Ning Zhu1, Andrew Lau1, Hisham Ibrahim1,2, Marwan Althagafi1,2, Kelly Tai1,4, Sharon J Hyduk1, Kateryna O Cybulsky1, Sherine Ensan1,4, Angela Li1,4, Rickvinder Besla1,2, Henry M Becker1,2,4, Haiyan Xiao1, Sanjiv A Luther5, Robert D Inman3,4,6, Clinton S Robbins1,2,4, Jenny Jongstra-Bilen1,2,4, Myron I Cybulsky1,2,4.
Abstract
Regions of the normal arterial intima predisposed to atherosclerosis are sites of ongoing monocyte trafficking and also contain resident myeloid cells with features of dendritic cells. However, the pathophysiological roles of these cells are poorly understood. Here we found that intimal myeloid cells underwent reverse transendothelial migration (RTM) into the arterial circulation after systemic stimulation of pattern-recognition receptors (PRRs). This process was dependent on expression of the chemokine receptor CCR7 and its ligand CCL19 by intimal myeloid cells. In mice infected with the intracellular pathogen Chlamydia muridarum, blood monocytes disseminated infection to the intima. Subsequent CCL19-CCR7-dependent RTM was critical for the clearance of intimal C. muridarum. This process was inhibited by hypercholesterolemia. Thus, RTM protects the normal arterial intima, and compromised RTM during atherogenesis might contribute to the intracellular retention of pathogens in atherosclerotic lesions.Entities:
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Year: 2016 PMID： 27668800 DOI： 10.1038/ni.3564
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606