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      Yolk Sac Macrophages, Fetal Liver, and Adult Monocytes Can Colonize an Empty Niche and Develop into Functional Tissue-Resident Macrophages.

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          Abstract

          Tissue-resident macrophages can derive from yolk sac macrophages (YS-Macs), fetal liver monocytes (FL-MOs), or adult bone-marrow monocytes (BM-MOs). The relative capacity of these precursors to colonize a niche, self-maintain, and perform tissue-specific functions is unknown. We simultaneously transferred traceable YS-Macs, FL-MOs, and BM-MOs into the empty alveolar macrophage (AM) niche of neonatal Csf2rb(-/-) mice. All subsets produced AMs, but in competition preferential outgrowth of FL-MOs was observed, correlating with their superior granulocyte macrophage-colony stimulating factor (GM-CSF) reactivity and proliferation capacity. When transferred separately, however, all precursors efficiently colonized the alveolar niche and generated AMs that were transcriptionally almost identical, self-maintained, and durably prevented alveolar proteinosis. Mature liver, peritoneal, or colon macrophages could not efficiently colonize the empty AM niche, whereas mature AMs could. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages and the plasticity of the mononuclear phagocyte system is largest at the precursor stage.

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          Author and article information

          Journal
          Immunity
          Immunity
          Elsevier BV
          1097-4180
          1074-7613
          Apr 19 2016
          : 44
          : 4
          Affiliations
          [1 ] Unit of Immunoregulation and Mucosal Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium; Department of Internal Medicine, Ghent University, Ghent 9000, Belgium.
          [2 ] Department of Internal Medicine, Ghent University, Ghent 9000, Belgium; Data Mining and Modeling for Systems Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium.
          [3 ] Unit of Immunoregulation and Mucosal Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent 9000, Belgium.
          [4 ] Department of Biomedical Molecular Biology, Ghent University, Ghent 9000, Belgium; Unit of Molecular Signal Transduction in Inflammation, VIB Inflammation Research Center, Ghent 9052, Belgium.
          [5 ] Unit of Immunoregulation and Mucosal Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium; Department of Internal Medicine, Ghent University, Ghent 9000, Belgium; Pulmonary Medicine, Erasmus University Medical Center, Rotterdam 3015CE, the Netherlands.
          [6 ] Unit of Immunoregulation and Mucosal Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent 9000, Belgium. Electronic address: martin.guilliams@ugent.be.
          Article
          S1074-7613(16)30055-3
          10.1016/j.immuni.2016.02.017
          26992565
          614cd53e-ded3-4a59-9254-32ceccf2050e
          History

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