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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma.

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dc.contributor.authorGomes, Ana L
dc.contributor.authorTeijeiro, Ana
dc.contributor.authorBurén, Stefan
dc.contributor.authorTummala, Krishna S
dc.contributor.authorYilmaz, Mahmut
dc.contributor.authorWaisman, Ari
dc.contributor.authorTheurillat, Jean-Philippe
dc.contributor.authorPerna, Cristian
dc.contributor.authorDjouder, Nabil
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderEuropean Foundation for the Study of Diabetes
dc.contributor.funderWorldwide Cancer Research
dc.date.accessioned2024-02-01T09:48:49Z
dc.date.available2024-02-01T09:48:49Z
dc.date.issued2016-07-11
dc.description.abstractObesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of the IL-17A receptor in myeloid cells. Human hepatitis, fatty liver, and viral hepatitis-associated HCC exhibit increased IL-17A correlating positively with steatosis. IL-17A blockers may prevent IR, NASH, and HCC in high-risk patients.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipWe thank the CNIO Biobank (M.J. Artiga and M. Morente) and Biobanco La Fe for collecting livers derived from obese patients and associated data used in this study. We are grateful to M. Rodriguez-Justo for analyzing some human HCCs as previously reported (Tummala et al., 2014) and to E. Wagner for critical reading of the manuscript. We are grateful to W. Krek for sharing URI antibodies previously reported (Tummala et al., 2014). We are thankful to the CNIO and the CCB program for sharing some reagents. A.L.G. was a recipientof the Caja Navarra postdoctoral fellowship. N.D. is a recipient of the Spanish Ramo´ n y Cajal fellowship. This work was supported by the CNIO-Severo Ochoa, the Spanish Ministry of Economy and Competitiveness (SAF2010 -18518 and SAF2013-46089-R), EFSD and WCR (AICR - 11-0242).es_ES
dc.format.number1es_ES
dc.format.page161es_ES
dc.format.volume30es_ES
dc.identifier.citationCancer Cell . 2016;30(1):161-175.es_ES
dc.identifier.doi10.1016/j.ccell.2016.05.020es_ES
dc.identifier.e-issn1878-3686es_ES
dc.identifier.journalCancer celles_ES
dc.identifier.pubmedID27411590es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17403
dc.language.isoenges_ES
dc.publisherCell Press
dc.relation.projectFISSAF2013-46089-Res_ES
dc.relation.projectFISSAF2010 - 18518es_ES
dc.relation.publisherversionhttps:\\10.1016/j.ccell.2016.05.020.es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Factores de Crecimiento, Nutrientes y Cánceres_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshAnimalses_ES
dc.subject.meshCarcinoma, Hepatocellulares_ES
dc.subject.meshDNA Damagees_ES
dc.subject.meshDiet, High-Fates_ES
dc.subject.meshGene Expression Regulation, Neoplastices_ES
dc.subject.meshHumanses_ES
dc.subject.meshInterleukin-17es_ES
dc.titleMetabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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