| Literature DB >> 31053503 |
Isabelle Mondor1, Myriam Baratin1, Marine Lagueyrie1, Lisa Saro1, Sandrine Henri1, Rebecca Gentek1, Delphine Suerinck1, Wolfgang Kastenmuller2, Jean X Jiang3, Marc Bajénoff4.
Abstract
In lymph nodes, subcapsular sinus macrophages (SSMs) form an immunological barrier that monitors lymph drained from peripheral tissues. Upon infection, SSMs activate B and natural killer T (NKT) cells while secreting inflammatory mediators. Here, we investigated the mechanisms regulating development and homeostasis of SSMs. Embryonic SSMs originated from yolk sac hematopoiesis and were replaced by a postnatal wave of bone marrow (BM)-derived monocytes that proliferated to establish the adult SSM network. The SSM network self-maintained by proliferation with minimal BM contribution. Upon pathogen-induced transient deletion, BM-derived cells contributed to restoring the SSM network. Lymphatic endothelial cells (LECs) were the main source of CSF-1 within the lymph node and conditional deletion of Csf1 in adult LECs decreased the network of SSMs and medullary sinus macrophages (MSMs). Thus, SSMs have a dual hematopoietic origin, and LECs are essential to the niche supporting these macrophages.Entities:
Keywords: colony stimulating factor-1; homeostasis; lymph node; macrophages; niche; ontogeny; stromal cells
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Year: 2019 PMID： 31053503 PMCID： PMC6697131 DOI： 10.1016/j.immuni.2019.04.002
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745