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dc.contributor.authorGonzález, Noelia A.-
dc.contributor.authorBensinger, Steven J.-
dc.contributor.authorDíaz, Mercedes-
dc.contributor.authorTontonoz, Peter-
dc.contributor.authorCastrillo, Antonio-
dc.date.accessioned2009-07-31T10:39:30Z-
dc.date.available2009-07-31T10:39:30Z-
dc.date.issued2009-07-30-
dc.identifier.citationImmunity 31(2): 245-258 (2009)en_US
dc.identifier.issn1074-7613-
dc.identifier.urihttp://hdl.handle.net/10261/15571-
dc.description14 pages, 7 figures.-- El pdf del artículo es el manuscrito de autor.-- et al.en_US
dc.descriptionSupporting information available at: http://www.cell.com/immunity/supplemental/S1074-7613(09)00318-5-
dc.description.abstractEffective clearance of apoptotic cells by macrophages is essential for immune homeostasis. The transcriptional pathways that allow macrophages to sense and respond to apoptotic cells are poorly defined. We found that liver X receptor (LXR) signaling was important for both apoptotic cell clearance and the maintenance of immune tolerance. Apoptotic cell engulfment activated LXR and thereby induced the expression of Mer, a receptor tyrosine kinase critical for phagocytosis. LXR-deficient macrophages exhibited a selective defect in phagocytosis of apoptotic cells and an aberrant proinflammatory response to them. As a consequence of these defects, mice lacking LXRs manifested a breakdown in self-tolerance and developed autoantibodies and autoimmune glomerulonephritis. Treatment with an LXR agonist ameliorated disease progression ina mouse model of lupus-like autoimmunity. Thus, activation of LXR by apoptotic cells engages a virtuous cycle that promotes their own clearance and couples engulfment to the suppression of inflammatory pathways.en_US
dc.description.sponsorshipThis work was supported by grants from the Spanish CSIC, MICINN of I+D SAF2005-03270 and 2008-00057, Ramón y Cajal Program, BM05- 228 from "La Caixa", 67/05 form FUNCIS and Ramón Areces Foundations to A.C. and from the NIH to P.T. (HL066088), P.E. (HL030568), and J.P. (HL049373). Flow cytometry was performed at the UCLA Core Facility supported by CA16042 and AI28697. Imaging was performed at the In Vivo Cellular and Molecular Imaging Center supported by EB001943 and CA92865.en_US
dc.format.extent131118 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.rightsopenAccessen_US
dc.titleApoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXRen_US
dc.typeartículoen_US
dc.identifier.doi10.1016/j.immuni.2009.06.018-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.immuni.2009.06.018en_US
dc.identifier.pmid19646905-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.languageiso639-1en-
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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