Stephen J. Jenkins

TL;DR: The tissue niche-specific factors that dictate cell phenotype are discussed, which will allow new strategies to promote the restoration of tissue homeostasis and explain why simplified models of macrophage activation do not explain the extent of heterogeneity seen in vivo.

TL;DR: It is revealed that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density, and expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.

TL;DR: Although monocyte-derived F4/80hi macrophages eventually displace the embryonic population with age in a process that is highly gender dependent and not due to proliferative exhaustion of the incumbent embryonic population, despite the greater proliferative activity of newly recruited cells.

TL;DR: IL-4 and CSF-1 both contribute to macrophages proliferation during nematode infection, but IL-4 permits increased tissue macrophage density without the coincident monocyte infiltration associated with elevated CSF1 levels.

TL;DR: It is shown that proliferation of both bone marrow-derived inflammatory and tissue resident macrophage lineage branches is a key feature of the inflammatory process with major implications for the mechanisms underlying recovery from inflammation.