RT Journal Article SR Electronic T1 Local Macrophage Proliferation, Rather than Recruitment from the Blood, Is a Signature of TH2 Inflammation JF Science JO Science FD American Association for the Advancement of Science SP 1284 OP 1288 DO 10.1126/science.1204351 VO 332 IS 6035 A1 Jenkins, Stephen J. A1 Ruckerl, Dominik A1 Cook, Peter C. A1 Jones, Lucy H. A1 Finkelman, Fred D. A1 van Rooijen, Nico A1 MacDonald, Andrew S. A1 Allen, Judith E. YR 2011 UL http://science.sciencemag.org/content/332/6035/1284.abstract AB 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 (TH2)–related pathologies under the control of the archetypal TH2 cytokine interleukin-4 (IL-4) and was a fundamental component of TH2 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.