Figure 2.

Model of the consequences of αvβ6 integrin-mediated activation of TGF-β by alveolar epithelial cells. Integrin expressed on the luminal surface can present active TGF-β to luminal macrophages, thereby inhibiting protease secretion and maintaining alveolar homeostasis. Integrin on the basal surface can present active TGF-β to fibroblasts, which in excess contributes to the development of pulmonary fibrosis, and to endothelial cells, which regulate pulmonary vascular permeability. Integrin on the lateral surface can present active TGF-β to adjacent epithelial cells, increasing epithelial permeability and decreasing the reabsorption of salt, and therefore water, from the alveolar space.