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-1β secretion, neutrophil extravasation, and loss of epithelial cells. In models of lung disease, inflammation and fibrosis can be controled 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.
Keywords: apoptosis, fas, inflammation, macrophage, lung, fibrosis, cell death, chemokines
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