Local Macrophage Proliferation, Rather than Recruitment from the Blood, Is a Signature of TH2 Inflammation

Stephen J Jenkins, Dominik Ruckerl, Peter C Cook, Lucy Jones, Fred D Finkelman, Nico van Rooijen, Andrew S MacDonald, Judith E Allen

Research output: Contribution to journalArticlepeer-review


A defining feature of inflammation is the accumulation of innate immune cells in the tissue that are thought to be recruited from the blood. We reveal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density. This inflammatory mechanism occurred during T helper 2 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 inflammation because exogenous IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal. Thus, expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.
Original languageEnglish
Pages (from-to)1284-1288
Number of pages5
Issue number6035
Publication statusPublished - 2011


  • Animals
  • Blood
  • Brugia malayi
  • Cell Proliferation
  • Female
  • Filariasis
  • Filarioidea
  • Inflammation
  • Interleukin-4
  • Macrophage Activation
  • Macrophages
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Monocytes
  • Th2 Cells


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