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dc.contributor.authorÁlvarez, Pilar-
dc.contributor.authorGenre, Fernanda-
dc.contributor.authorIglesias, Marcos-
dc.contributor.authorAugustin, Juan Jesús-
dc.contributor.authorTamayo, Esther-
dc.contributor.authorEscolà-Gil, Joan Carles-
dc.contributor.authorLavín, Bernardo-
dc.contributor.authorBlanco-Vaca, Francisco-
dc.contributor.authorMerino, Ramón-
dc.contributor.authorMerino, Jesús-
dc.date.accessioned2018-05-08T10:59:02Z-
dc.date.available2018-05-08T10:59:02Z-
dc.date.issued2016-
dc.identifierdoi: 10.1111/cei.12857-
dc.identifiere-issn: 1365-2249-
dc.identifierissn: 0009-9104-
dc.identifier.citationClinical and Experimental Immunology 186(3): 292-303 (2016)-
dc.identifier.urihttp://hdl.handle.net/10261/164542-
dc.description.abstractApolipoprotein E (ApoE) deficiency promoted an exacerbation of autoimmune arthritis in mice by inducing proinflammatory immune responses. In this study we analysed the contribution of hypercholesterolaemia and/or the absence of ApoE anti-inflammatory properties, unrelated to its function in the control of cholesterol metabolism, towards the acceleration of arthritis in these mutant animals. The induction and severity of collagen type II-induced arthritis (CIA) were compared for B10.RIII wild-type (WT), B10.RIII.ApoE, B10.RIII.ApoE and B10.RIII.low-density lipoprotein receptor (LDLR) mice with different concentrations of circulating ApoE and cholesterol. A 50–70% reduction in serum levels of ApoE was observed in heterozygous B10.RIII.ApoE mice in comparison to B10.RIII.WT, although both strains of mice exhibited similar circulating lipid profiles. This ApoE reduction was associated with an increased CIA severity that remained lower than in homozygous B10.RIII.ApoE mice. An important rise in circulating ApoE concentration was observed in hypercholesterolaemic B10.RIII.LDLR mice fed with a normal chow diet, and both parameters increased further with an atherogenic hypercholesterolaemic diet. However, the severity of CIA in B10.RIII.LDLR mice was similar to that of B10.RIII.WT controls. In conclusion, by comparing the evolution of CIA between several strains of mutant mice with different levels of serum ApoE and cholesterol, our results demonstrate that both hypercholesterolaemia and ApoE regulate the intensity of in-vivo systemic autoimmune responses.-
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministerio de Economía y Competitividad to J. M. (SAF2012‐34059) and R. M. (SAF2014‐55088‐R), which were co‐funded by the European Regional Development Fund. M. I. was supported partially by a grant from the Spanish Ministerio de Economía y Competitividad (IPT2011‐1527‐010000) associated with fibrostatin SL.-
dc.publisherJohn Wiley & Sons-
dc.publisherBritish Society for Immunology-
dc.relationMINECO/ICTI2013-2016/SAF2014‐55088‐R-
dc.relation.isversionofPostprint-
dc.rightsopenAccess-
dc.subjectApoE-
dc.subjectLDLR-
dc.subjectCollagen type II-induced arthritis-
dc.subjectHypercholesterolaemia-
dc.titleModulation of autoimmune arthritis severity in mice by apolipoprotein E (ApoE) and cholesterol-
dc.typeartículo-
dc.identifier.doi10.1111/cei.12857-
dc.relation.publisherversionhttps://doi.org/10.1111/cei.12857-
dc.date.updated2018-05-08T10:59:02Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderFibrostatin-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderEuropean Commission-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.pmid27571306-
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