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
Current Drug Targets - Inflammation & Allergy
Title: Role of Fas-Ligand Induced Apoptosis in Pulmonary Inflammation and Injury
Volume: 2 Issue: 2
Author(s): George A. DosReis and Valeria M. Borges
Affiliation:
Keywords: apoptosis, fas, inflammation, macrophage, lung, fibrosis, cell death, chemokines
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.
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Cite this article as:
DosReis A. George and Borges M. Valeria, Role of Fas-Ligand Induced Apoptosis in Pulmonary Inflammation and Injury, Current Drug Targets - Inflammation & Allergy 2003; 2 (2) . https://dx.doi.org/10.2174/1568010033484287
DOI https://dx.doi.org/10.2174/1568010033484287 |
Print ISSN 1568-010X |
Publisher Name Bentham Science Publisher |
Online ISSN 1568-010X |
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