Recent investigations have highlighted new roles for the macrophage (M_ϕ) in the biology of inflammation. Selective depletion of M_ϕs from inflamed sites has confirmed their predominant role in immune-mediated damage. The components of this injury have been dissected. M_ϕs mediate death of stromal, parenchymal and other immune cells by engaging the death programme, resulting in apoptosis. In addition, M_ϕs induce destruction of matrix and extracellular structures both directly and indirectly by inducing stromal cells to release matrix metalloproteinases. However, there is another side to the inflammatory M_ϕ. Evidence is provided that M_ϕs at the same sites possess the ability to aid cell proliferation, secrete and stabilize new matrix components and induce resident cells to secrete matrix components themselves. M_ϕ phagocytosis of apoptotic cells brings about a change from the cell-killing matrix-degrading cell to the matrix-generating cell-proliferating tissue-healing cell. Just as both M_ϕ types are necessary at the inflamed site, the right balance of these two populations is required for healing and resolution. Evidence of excessive inflammation as a manifestation of impaired phagocytosis of apoptotic cells emphasizes that defects in the transition from one M_ϕ type to another may account for the uncontrolled excessive inflammation seen in disease. Recent insights into the mechanisms by which apoptotic cells signal the change of function to the M_ϕ offer the prospect of novel targets for manipulation of M_ϕs in the inflamed tissue.