Role of Fas-ligand induced apoptosis in pulmonary inflammation and injury.
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.
DosReis
George A
GA
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21949-900, Brazil. gdosreis@biof.ufrj.br
Borges
Valeria M
VM
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053222:Fas Ligand Protein; D005786:Gene Expression Regulation / Q000502:physiology; D006801:Humans; D008171:Lung Diseases / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D008562:Membrane Glycoproteins / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology; D011014:Pneumonia / Q000139:chemically induced / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D011658:Pulmonary Fibrosis / Q000235:genetics / Q000473:pathology / Q000503:physiopathology
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins