The central role of Fas-ligand cell signaling in inflammatory lung diseases.
Autor(a) principal: | |
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Data de Publicação: | 2004 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da FIOCRUZ (ARCA) |
Texto Completo: | https://www.arca.fiocruz.br/handle/icict/9472 |
Resumo: | Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil |
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DosReis, George AlexandreBorges, Valeria de MatosZin, Walter Araujo2015-02-10T14:22:32Z2015-02-10T14:22:32Z2004DosREIS, G. A.; BORGES, V. M.; ZIN, W. A. The central role of Fas-ligand cell signaling in inflammatory lung diseases. Journal of Cellular and Molecular Medicina, v. 8, n. 3, p. 285-293, 2004.1582-1838https://www.arca.fiocruz.br/handle/icict/9472engopen accessThe central role of Fas-ligand cell signaling in inflammatory lung diseases.info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleFederal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilFederal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, BrasilFollowing 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 diseasesFas ligandApoptosisInflammationNeutrophilMacrophagePhagocytosisFibrosisLungInjurySilicosisAntígenos CD95/imunologiaGlicoproteínas de Membrana/fisiologiaPneumonia/imunologiaDoença AgudaApoptoseCélulas Epiteliais/metabolismoProteína Ligante FasRegulação da Expressão GênicaHumanosInterleucina-1/metabolismoMacrófagos Alveolares/imunologiaNeutrófilos/imunologiaPneumonia/metabolismoAlvéolos Pulmonares/imunologiaFibrose Pulmonar/imunologiaTransdução de SinalSilicose/imunologiainfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da FIOCRUZ (ARCA)instname:Fundação Oswaldo Cruz (FIOCRUZ)instacron:FIOCRUZTHUMBNAILDosReis GA The central...pdf.jpgDosReis GA The central...pdf.jpgGenerated Thumbnailimage/jpeg1531https://www.arca.fiocruz.br/bitstream/icict/9472/4/DosReis%20GA%20The%20central...pdf.jpg74eff2014a6f5538872b8857c8089dd4MD54LICENSElicense.txtlicense.txttext/plain; charset=utf-81914https://www.arca.fiocruz.br/bitstream/icict/9472/1/license.txt7d48279ffeed55da8dfe2f8e81f3b81fMD51ORIGINALDosReis GA The central...pdfDosReis GA The central...pdfapplication/pdf1398350https://www.arca.fiocruz.br/bitstream/icict/9472/2/DosReis%20GA%20The%20central...pdf38fc272d7e226f14c4c4eb70ec8b5764MD52TEXTDosReis GA The central...pdf.txtDosReis GA The central...pdf.txtExtracted texttext/plain34522https://www.arca.fiocruz.br/bitstream/icict/9472/3/DosReis%20GA%20The%20central...pdf.txtb679414363cf14293021d5ff139304e0MD53icict/94722023-03-15 14:32:47.513oai:www.arca.fiocruz.br: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ório InstitucionalPUBhttps://www.arca.fiocruz.br/oai/requestrepositorio.arca@fiocruz.bropendoar:21352023-03-15T17:32:47Repositório Institucional da FIOCRUZ (ARCA) - Fundação Oswaldo Cruz (FIOCRUZ)false |
dc.title.pt_BR.fl_str_mv |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
title |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
spellingShingle |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. DosReis, George Alexandre Fas ligand Apoptosis Inflammation Neutrophil Macrophage Phagocytosis Fibrosis Lung Injury Silicosis Antígenos CD95/imunologia 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 |
title_short |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
title_full |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
title_fullStr |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
title_full_unstemmed |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
title_sort |
The central role of Fas-ligand cell signaling in inflammatory lung diseases. |
author |
DosReis, George Alexandre |
author_facet |
DosReis, George Alexandre Borges, Valeria de Matos Zin, Walter Araujo |
author_role |
author |
author2 |
Borges, Valeria de Matos Zin, Walter Araujo |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
DosReis, George Alexandre Borges, Valeria de Matos Zin, Walter Araujo |
dc.subject.en.pt_BR.fl_str_mv |
Fas ligand Apoptosis Inflammation Neutrophil Macrophage Phagocytosis Fibrosis Lung Injury Silicosis |
topic |
Fas ligand Apoptosis Inflammation Neutrophil Macrophage Phagocytosis Fibrosis Lung Injury Silicosis Antígenos CD95/imunologia 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 |
dc.subject.decs.pt_BR.fl_str_mv |
Antígenos CD95/imunologia 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 |
description |
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil |
publishDate |
2004 |
dc.date.issued.fl_str_mv |
2004 |
dc.date.accessioned.fl_str_mv |
2015-02-10T14:22:32Z |
dc.date.available.fl_str_mv |
2015-02-10T14:22:32Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
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article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
DosREIS, G. A.; BORGES, V. M.; ZIN, W. A. The central role of Fas-ligand cell signaling in inflammatory lung diseases. Journal of Cellular and Molecular Medicina, v. 8, n. 3, p. 285-293, 2004. |
dc.identifier.uri.fl_str_mv |
https://www.arca.fiocruz.br/handle/icict/9472 |
dc.identifier.issn.none.fl_str_mv |
1582-1838 |
identifier_str_mv |
DosREIS, G. A.; BORGES, V. M.; ZIN, W. A. The central role of Fas-ligand cell signaling in inflammatory lung diseases. Journal of Cellular and Molecular Medicina, v. 8, n. 3, p. 285-293, 2004. 1582-1838 |
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open access |
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open access |
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