The body's first response to injury is an inflammatory one that aims to clear the responsible agent rapidly and effectively. At some point, however, the tissue damage that results from both the initial stimulus and the pro-inflammatory environment must be repaired. An important part of this healing process is tissue fibrosis, in which connective tissue replaces parenchymal tissue. However, as Thomas Wynn discusses on page 583, in some cases, this tissue remodelling can continue unchecked and can lead to the formation of pathogenic scar tissue. Given the high incidence of fibrotic disorders affecting all major organs, it is essential for the development of targeted therapies that we learn more about the relationship between persistent inflammation and fibrogenesis.

On page 617, William Parks and colleagues also discuss the links between inflammation and tissue repair. They discuss how matrix metalloproteinases — which are best known for their role in turnover and degradation of the extracellular matrix — can also regulate the inflammatory process through their effects on the activity of cytokines and chemokines, and they suggest that the programmes regulating repair and inflammation might have co-evolved.

Jukka Vakkila and Michael Lotze (page 641) take the implications of chronic inflammation one step further by putting forward their opinion that sustained inflammatory processes in adults can lead to cancer. The rounds of cell proliferation and necrosis that occur at sites of inflammation, associated with epigenetic changes that silence tumour-suppressor genes, set the scene for the accumulation of further mutations and tumour growth. Targeting inflammatory cells such as dendritic cells and natural killer cells, which are known to infiltrate many solid tumours, might therefore offer new hope for cancer therapies.