Artigo Acesso aberto Revisado por pares

Self-renewing resident arterial macrophages arise from embryonic CX3CR1+ precursors and circulating monocytes immediately after birth

2015; Nature Portfolio; Volume: 17; Issue: 2 Linguagem: Inglês

10.1038/ni.3343

ISSN

1529-2916

Autores

Sherine Ensan, Angela Li, Rickvinder Besla, Norbert Degousée, Jake Cosme, Mark Roufaiel, Eric A. Shikatani, Mahmoud El-Maklizi, Jesse W. Williams, Lauren Robins, Cedric C Li, Bonnie J.B. Lewis, Tae Jin Yun, Jun Seong Lee, Peter Wieghofer, Ramzi Khattar, Kaveh Farrokhi, John Byrne, Maral Ouzounian, Caleb C. J. Zavitz, Gary Levy, Carla M. T. Bauer, Peter Libby, Mansoor Husain, Filip K. Świrski, Cheolho Cheong, Marco Prinz, Ingo Hilgendorf, Gwendalyn J. Randolph, Slava Epelman, Anthony O. Gramolini, Myron I. Cybulsky, Barry B. Rubin, Clinton S. Robbins,

Tópico(s)

Neuroinflammation and Neurodegeneration Mechanisms

Resumo

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.

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