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https://www.arca.fiocruz.br/handle/icict/9472
THE CENTRAL ROLE OF FAS-LIGAND CELL SIGNALING IN INFLAMMATORY LUNG DISEASES.
Apoptosis
Inflammation
Neutrophil
Macrophage
Phagocytosis
Fibrosis
Lung
Injury
Silicosis
Glicoproteínas de Membrana/fisiologia
Pneumonia/imunologia
Doença Aguda
Apoptose
Células Epiteliais/metabolismo
Proteína Ligante Fas
Regulação da Expressão Gênica
Humanos
Interleucina-1/metabolismo
Macrófagos Alveolares/imunologia
Neutrófilos/imunologia
Pneumonia/metabolismo
Alvéolos Pulmonares/imunologia
Fibrose Pulmonar/imunologia
Transdução de Sinal
Silicose/imunologia
Affilliation
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Abstract
Following inflammation and injury in the lung, loss of epithelial cell precursors could determine the balance between tissue regeneration and fibrosis. This review discusses evidence that proapoptotic Fas-Fas ligand (FasL) signaling plays a central role in pulmonary inflammation, injury and fibrosis. FasL signaling induces inflammatory apoptosis in epithelial cells and alveolar macrophages, with concomitant IL-1 beta and chemokine release, leading to neutrophil infiltration. FasL signaling plays a critical role in models of acute lung injury, idiopathic pulmonary fibrosis and silicosis; blockade of Fas-FasL interactions either prevents or attenuates pulmonary inflammation and fibrosis. Serologic and immunohistochemical studies in patients support a major pathogenic role of Fas and FasL molecules in inflammatory lung diseases. Identification of the pathogenic role of FasL could facilitate the discovery of more effective treatments for currently untreatable inflammatory lung diseases
Keywords
Fas ligandApoptosis
Inflammation
Neutrophil
Macrophage
Phagocytosis
Fibrosis
Lung
Injury
Silicosis
DeCS
Antígenos CD95/imunologiaGlicoproteínas de Membrana/fisiologia
Pneumonia/imunologia
Doença Aguda
Apoptose
Células Epiteliais/metabolismo
Proteína Ligante Fas
Regulação da Expressão Gênica
Humanos
Interleucina-1/metabolismo
Macrófagos Alveolares/imunologia
Neutrófilos/imunologia
Pneumonia/metabolismo
Alvéolos Pulmonares/imunologia
Fibrose Pulmonar/imunologia
Transdução de Sinal
Silicose/imunologia
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