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dc.contributor.authorHerranz, Sandra 
dc.contributor.authorTravés, Paqui G
dc.contributor.authorLuque, Alfonso 
dc.contributor.authorHortelano, Sonsoles 
dc.date.accessioned2021-04-29T10:53:19Z
dc.date.available2021-04-29T10:53:19Z
dc.date.issued2012-11-30
dc.identifier.citationOncoimmunology. 2012;1(8):1227-1238.es_ES
dc.identifier.issn2162-4011es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12825
dc.description.abstractThe ARF locus is frequently inactivated in human cancer. The oncosuppressor ARF has indeed been described as a general sensor for different situation of cellular stress. We have previously demonstrated that ARF deficiency severely impairs inflammatory responses in vitro and in vivo, establishing a role for ARF in the regulation of innate immunity. The aim of the present work was to get further insights into the immune functions of ARF and to evaluate its possible contribution to the polarization of macrophages toward the M1 or M2 phenotype. Our results demonstrate that resting Arf(-/-) macrophages express high levels of Ym1 and Fizz-1, two typical markers of alternatively-activated macrophages (M2). Additionally, Arf(-/-) peritoneal macrophages showed an impaired response to lipopolysaccharide (a classical inducer of M1 polaryzation) and a reduced production of pro-inflammatory cytokines/chemokines. Moreover, upon stimulation with interleukin-4 (IL-4), an inducer of the M2 phenotype, well established M2 markers such as Fizz-1, Ym1 and arginase-1 were upregulated in Arf(-/-) as compared with wild type macrophages. Accordingly, the cytokine and chemokine profile associated with the M2 phenotype was significantly overexpressed in Arf(-/-) macrophages responding to IL-4. In addition, multiple pro-angiogenic factors such as VEGF and MMP-9 were also increased. In summary, these results indicate that ARF contributes to the polarization and functional plasticity of macrophages.es_ES
dc.description.sponsorshipThis study was supported by grant PI11.0036 from the FIS and MPY 1410/09 from ISCIII to S.H.es_ES
dc.language.isoenges_ES
dc.publisherTaylor & Francis es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.subjectARFes_ES
dc.subjectIL-4es_ES
dc.subjectTAMses_ES
dc.subjectAlternative activationes_ES
dc.subjectMacrophagees_ES
dc.titleRole of the tumor suppressor ARF in macrophage polarization: Enhancement of the M2 phenotype in ARF-deficient mice.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial 4.0 Internacional*
dc.identifier.pubmedID23243586es_ES
dc.format.volume1es_ES
dc.format.number8es_ES
dc.format.page1227-1238es_ES
dc.identifier.doi10.4161/onci.21207es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.4161/onci.21207es_ES
dc.identifier.journalOncoimmunologyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI11.0036es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MPY1410/09es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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