Role of Fas-ligand induced apoptosis in pulmonary inflammation and injury

Abstract

In the lung, inflammation followed by the loss of epithelial cell precursors beyond a safeguard threshold, leads to increased mesenchymal repair and autonomous fibrosis. Fas-Fas ligand induced apoptosis promotes IL-1beta secretion, neutrophil extravasation, and loss of epithelial cells. In models of lung disease, inflammation and fibrosis can be controlled by interfering with either Fas-Fas ligand interaction, or with downstream caspase activation. These results suggest that the Fas-Fas ligand pathway is a target for the design of new therapeutic strategies for lung diseases.