RT Journal Article
SR Electronic
T1 Local Macrophage Proliferation, Rather than Recruitment from the Blood, Is a Signature of T<sub>H</sub>2 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.