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

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    Rights statement: *This manuscript has been accepted for publication in Science. This version has not undergone final editing. Please refer to the complete version of record at http://www.sciencemag.org/.

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http://www.sciencemag.org/content/332/6035/1284
Original languageEnglish
Pages (from-to)1284-1288
Number of pages5
JournalScience
Volume332
Issue number6035
DOIs
Publication statusPublished - 2011

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.

    Research areas

  • 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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