Damage to any tissue triggers a cascade of events that leads to rapid repair of the wound - if the tissue is skin, then repair involves re-epithelialization, formation of granulation tissue and contraction of underlying wound connective tissues. This concerted effort by the wounded cell layers is accompanied by, and might also be partially regulated by, a robust inflammatory response, in which first neutrophils and then macrophages and mast cells emigrate from nearby tissues and from the circulation. Clearly, this inflammatory response is crucial for fighting infection and must have been selected for during the course of evolution so that tissue damage did not inevitably lead to death through septicemia. But, aside from this role, exactly what are the functions of the various leukocyte lineages that are recruited with overlapping time courses to the wound site, and might they do more harm than good? Recent knockout and knockdown studies suggest that depletion of one or more of the inflammatory cell lineages can even enhance healing, and we discuss new views on how regulation of the migration of inflammatory cells to sites of tissue damage might guide therapeutic strategies for modulating the inflammatory response.