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Science. 2011 Jun 10;332(6035):1284-8. doi: 10.1126/science.1204351. Epub 2011 May 12.

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

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  • 1Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK.

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.

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PMID:
21566158
[PubMed - indexed for MEDLINE]
PMCID:
PMC3128495
Free PMC Article

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