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Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation

Research output: Contribution to journalJournal articlepeer-review

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  • Stephen J Jenkins
  • Dominik Ruckerl
  • Peter C Cook
  • Lucy H Jones
  • Fred D Finkelman
  • Nico van Rooijen
  • Andrew S MacDonald
  • Judith E Allen
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<mark>Journal publication date</mark>10/06/2011
<mark>Journal</mark>Science
Issue number6035
Volume332
Number of pages5
Pages (from-to)1284-1288
Publication StatusPublished
<mark>Original language</mark>English

Abstract

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.