File:Schematic representation of macrophage plasticity and its involvement in tissue injury.png

English: Macrophages recruited to the site of an injury or infection during the initiation phase of the inflammatory reaction have an M1 phenotype. They produce pro-inflammatory and stress mediators and cytokines, such as tumor necrosis factor α (TNFα), interleukin (IL)-1 and -12, interferon γ (IFNγ), an enzyme generating nitric oxide (iNOS), and reactive oxygen species (ROS). These macrophages have proinflammatory and antimicrobial effects and lead to matrix degradation and tissue destruction. During the resolution phase of the injury, these M1 macrophages are converted into an M2 phenotype with a different cytokine and chemokine repertoire, including IL-10, transforming growth factor β (TGF-β), matrix metalloproteinases (MMPs), arginase 1 (Arg1), tissue inhibitors of metalloproteinases (TIMPs), and vascular epithelial growth factor (VEGF). These M2 macrophages have anti-inflammatory effects and promote blood-vessel formation (angiogenesis), matrix synthesis, and tissue remodeling.