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Article: Fatal Hepatitis Mediated by Tumor Necrosis Factor TNFα Requires Caspase-8 and Involves the BH3-Only Proteins Bid and Bim

TitleFatal Hepatitis Mediated by Tumor Necrosis Factor TNFα Requires Caspase-8 and Involves the BH3-Only Proteins Bid and Bim
Authors
KeywordsMOLIMMUNO
Issue Date2009
Citation
Immunity, 2009, v. 30, n. 1, p. 56-66 How to Cite?
AbstractApoptotic death of hepatocytes, a contributor to many chronic and acute liver diseases, can be a consequence of overactivation of the immune system and is often mediated by TNFα. Injection with lipopolysaccharide (LPS) plus the transcriptional inhibitor D(+)-galactosamine (GalN) or mitogenic T cell activation causes fatal hepatocyte apoptosis in mice, which is mediated by TNFα, but the effector mechanisms remain unclear. Our analysis of gene-targeted mice showed that caspase-8 is essential for hepatocyte killing in both settings. Loss of Bid, the proapoptotic BH3-only protein activated by caspase-8 and essential for Fas ligand-induced hepatocyte killing, resulted only in a minor reduction of liver damage. However, combined loss of Bid and another BH3-only protein, Bim, activated by c-Jun N-terminal kinase (JNK), protected mice from LPS+GalN-induced hepatitis. These observations identify caspase-8 and the BH3-only proteins Bid and Bim as potential therapeutic targets for treatment of inflammatory liver diseases. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/291872
ISSN
2023 Impact Factor: 25.5
2023 SCImago Journal Rankings: 13.578
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKaufmann, Thomas-
dc.contributor.authorJost, Philipp J.-
dc.contributor.authorPellegrini, Marc-
dc.contributor.authorPuthalakath, Hamsa-
dc.contributor.authorGugasyan, Raffi-
dc.contributor.authorGerondakis, Steve-
dc.contributor.authorCretney, Erika-
dc.contributor.authorSmyth, Mark J.-
dc.contributor.authorSilke, John-
dc.contributor.authorHakem, Razq-
dc.contributor.authorBouillet, Philippe-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorDixit, Vishva M.-
dc.contributor.authorStrasser, Andreas-
dc.date.accessioned2020-11-17T14:55:17Z-
dc.date.available2020-11-17T14:55:17Z-
dc.date.issued2009-
dc.identifier.citationImmunity, 2009, v. 30, n. 1, p. 56-66-
dc.identifier.issn1074-7613-
dc.identifier.urihttp://hdl.handle.net/10722/291872-
dc.description.abstractApoptotic death of hepatocytes, a contributor to many chronic and acute liver diseases, can be a consequence of overactivation of the immune system and is often mediated by TNFα. Injection with lipopolysaccharide (LPS) plus the transcriptional inhibitor D(+)-galactosamine (GalN) or mitogenic T cell activation causes fatal hepatocyte apoptosis in mice, which is mediated by TNFα, but the effector mechanisms remain unclear. Our analysis of gene-targeted mice showed that caspase-8 is essential for hepatocyte killing in both settings. Loss of Bid, the proapoptotic BH3-only protein activated by caspase-8 and essential for Fas ligand-induced hepatocyte killing, resulted only in a minor reduction of liver damage. However, combined loss of Bid and another BH3-only protein, Bim, activated by c-Jun N-terminal kinase (JNK), protected mice from LPS+GalN-induced hepatitis. These observations identify caspase-8 and the BH3-only proteins Bid and Bim as potential therapeutic targets for treatment of inflammatory liver diseases. © 2009 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofImmunity-
dc.subjectMOLIMMUNO-
dc.titleFatal Hepatitis Mediated by Tumor Necrosis Factor TNFα Requires Caspase-8 and Involves the BH3-Only Proteins Bid and Bim-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.immuni.2008.10.017-
dc.identifier.pmid19119023-
dc.identifier.pmcidPMC2938743-
dc.identifier.scopuseid_2-s2.0-58149262908-
dc.identifier.volume30-
dc.identifier.issue1-
dc.identifier.spage56-
dc.identifier.epage66-
dc.identifier.isiWOS:000262769900010-
dc.identifier.issnl1074-7613-

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