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The STAT3–IL-10–IL-6 Pathway Is a Novel Regulator of Macrophage Efferocytosis and Phenotypic Conversion in Sterile Liver Injury

Research output: Contribution to journalArticle

  • Lara Campana
  • Philip J Starkey Lewis
  • Antonella Pellicoro
  • Rebecca L Aucott
  • Janet Man
  • Eoghan O'Duibhir
  • Sarah E Mok
  • Sofia Ferreira-Gonzalez
  • Eilidh Livingstone
  • Stephen N Greenhalgh
  • Katherine L Hull
  • Douglas Vernimmen
  • Neil C Henderson
  • Luke Boulter
  • Christopher D Gregory
  • Yi Feng
  • Stephen M Anderton
  • Stuart J Forbes
  • John P Iredale
Original languageEnglish
Pages (from-to)1169-1187
Number of pages19
JournalJournal of Immunology
Issue number3
Early online date22 Jan 2018
DateAccepted/In press - 25 Nov 2017
DateE-pub ahead of print - 22 Jan 2018
DatePublished (current) - 1 Feb 2018


The disposal of apoptotic bodies by professional phagocytes is crucial to effective inflammation resolution. Our ability to improve the disposal of apoptotic bodies by professional phagocytes is impaired by a limited understanding of the molecular mechanisms that regulate the engulfment and digestion of the efferocytic cargo. Macrophages are professional phagocytes necessary for liver inflammation, fibrosis, and resolution, switching their phenotype from proinflammatory to restorative. Using sterile liver injury models, we show that the STAT3–IL-10–IL-6 axis is a positive regulator of macrophage efferocytosis, survival, and phenotypic conversion, directly linking debris engulfment to tissue repair.

Additional information

Copyright © 2018 by The American Association of Immunologists, Inc.

    Research areas

  • Adoptive Transfer, Animals, Apoptosis/immunology, Humans, Interleukin-10/metabolism, Interleukin-6/metabolism, Liver/injuries, Liver Cirrhosis/pathology, Macrophages/immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Necrosis/immunology, Phagocytosis/immunology, Regeneration/physiology, STAT3 Transcription Factor/metabolism, Zebrafish/embryology



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