| Literature DB >> 26642357 |
Sherine Ensan1, Angela Li1, Rickvinder Besla2, Norbert Degousee3, Jake Cosme3, Mark Roufaiel3, Eric A Shikatani2, Mahmoud El-Maklizi1, Jesse W Williams4, Lauren Robins3, Cedric Li3, Bonnie Lewis3, Tae Jin Yun5, Jun Seong Lee5, Peter Wieghofer6, Ramzi Khattar3, Kaveh Farrokhi1, John Byrne3,7, Maral Ouzounian3,7, Caleb C J Zavitz3, Gary A Levy1,3, Carla M T Bauer8, Peter Libby9, Mansoor Husain2,3,7, Filip K Swirski10, Cheolho Cheong5, Marco Prinz11, Ingo Hilgendorf12, Gwendalyn J Randolph4, Slava Epelman1,3,7, Anthony O Gramolini3,7,7, Myron I Cybulsky2,3,7, Barry B Rubin3,7, Clinton S Robbins1,2,3,7.
Abstract
Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from CX3CR1(+) precursors and postnatally from bone marrow-derived monocytes that colonize the tissue immediately after birth. In adulthood, proliferation (rather than monocyte recruitment) sustains arterial macrophages in the steady state and after severe depletion following sepsis. After infection, arterial macrophages return rapidly to functional homeostasis. Finally, survival of resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.Entities:
Mesh：
Substances：
Year: 2015 PMID： 26642357 DOI： 10.1038/ni.3343
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606