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Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation

Author

Listed:
  • Luke C. Davies

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

  • Marcela Rosas

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

  • Stephen J. Jenkins

    (Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh)

  • Chia-Te Liao

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

  • Martin J. Scurr

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

  • Frank Brombacher

    (International Center for Genetic Engineering and Biotechnology
    Institute of Infectious Disease and Molecular Medicine, University of Cape Town)

  • Donald J. Fraser

    (Institute of Molecular and Experimental Medicine, Cardiff University School of Medicine)

  • Judith E. Allen

    (Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh)

  • Simon A. Jones

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

  • Philip R. Taylor

    (Institute of Infection and Immunity, Cardiff University School of Medicine)

Abstract

The general paradigm is that monocytes are recruited to sites of inflammation and terminally differentiate into macrophages. There has been no demonstration of proliferation of peripherally-derived inflammatory macrophages under physiological conditions. Here we show that proliferation of both bone marrow-derived inflammatory and tissue-resident macrophage lineage branches is a key feature of the inflammatory process with major implications for the mechanisms underlying recovery from inflammation. Both macrophage lineage branches are dependent on M-CSF during inflammation, and thus the potential for therapeutic interventions is marked. Furthermore, these observations are independent of Th2 immunity. These studies indicate that the proliferation of distinct macrophage populations provides a general mechanism for macrophage expansion at key stages during inflammation, and separate control mechanisms are implicated.

Suggested Citation

  • Luke C. Davies & Marcela Rosas & Stephen J. Jenkins & Chia-Te Liao & Martin J. Scurr & Frank Brombacher & Donald J. Fraser & Judith E. Allen & Simon A. Jones & Philip R. Taylor, 2013. "Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation," Nature Communications, Nature, vol. 4(1), pages 1-10, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2877
    DOI: 10.1038/ncomms2877
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    Cited by:

    1. Dhanashree Surve & Adam Fish & Maharshi Debnath & Aniruddha Pinjari & Adrian Lorenzana & Sumi Piya & Shelly Peyton & Ashish Kulkarni, 2024. "Sprayable inflammasome-inhibiting lipid nanorods in a polymeric scaffold for psoriasis therapy," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    2. Han-Ying Huang & Yan-Zhou Chen & Chuang Zhao & Xin-Nan Zheng & Kai Yu & Jia-Xing Yue & Huai-Qiang Ju & Yan-Xia Shi & Lin Tian, 2024. "Alternations in inflammatory macrophage niche drive phenotypic and functional plasticity of Kupffer cells," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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