JOURNAL ARTICLE

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

Stephen J Jenkins, Dominik Ruckerl, Peter C Cook, Lucy H Jones, Fred D Finkelman, Nico van Rooijen, Andrew S MacDonald, Judith E Allen
Science 2011 June 10, 332 (6035): 1284-8
21566158
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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