Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/54614
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dc.contributor.authorHong, Cynthia
dc.contributor.authorKidani, Yoko
dc.contributor.authorA-Gonzalez, Noelia
dc.contributor.authorPhung, Tram
dc.contributor.authorIto, Ayaka
dc.contributor.authorRong, Xin
dc.contributor.authorEricson, Katrin
dc.contributor.authorMikkola, Hanna
dc.contributor.authorBeaven, Simon W.
dc.contributor.authorMiller, Lloyd S.
dc.contributor.authorShao, Wen Hai
dc.contributor.authorCohen, Philip L.
dc.contributor.authorCastrillo, Antonio
dc.contributor.authorTontonoz, Peter
dc.contributor.authorBensinger, Steven J.
dc.date.accessioned2019-02-18T11:58:07Z-
dc.date.available2019-02-18T11:58:07Z-
dc.date.issued2012
dc.identifier.issn0021-9738
dc.identifier.urihttp://hdl.handle.net/10553/54614-
dc.description.abstractThe most abundant immune cell type is the neutrophil, a key first responder after pathogen invasion. Neutrophil numbers in the periphery are tightly regulated to prevent opportunistic infections and aberrant inflammation. In healthy individuals, more than 1 x 10(9) neutrophils per kilogram body weight are released from the bone marrow every 24 hours. To maintain homeostatic levels, an equivalent number of senescent cells must be cleared from circulation. Recent studies indicate that clearance of senescent neutrophils by resident tissue macrophages and DCs helps to set homeostatic levels of neutrophils via effects on the IL-23/IL-17/G-CSF cytokine axis, which stimulates neutrophil production in the bone marrow. However, the molecular events in phagocytes underlying this feedback loop have remained indeterminate. Liver X receptors (LXRs) are members of the nuclear receptor superfamily that regulate both lipid metabolic and inflammatory gene expression. Here, we demonstrate that LXRs contribute to the control of neutrophil homeostasis. Using gain- and loss-of-function models, we found that LXR signaling regulated the efficient clearance of senescent neutrophils by peripheral tissue APCs in a Mer-dependent manner. Furthermore, activation of LXR by engulfed neutrophils directly repressed the IL-23/IL-17/G-CSF granulopoietic cytokine cascade. These results provide mechanistic insight into the molecular events orchestrating neutrophil homeostasis and advance our understanding of LXRs as integrators of phagocyte function, lipid metabolism, and cytokine gene expression.
dc.publisher0021-9738
dc.relation.ispartofJournal of Clinical Investigation
dc.sourceJournal of Clinical Investigation[ISSN 0021-9738],v. 122, p. 337-347
dc.subject.otherBone-Marrow
dc.subject.otherApoptotic Neutrophils
dc.subject.otherNuclear Receptors
dc.subject.otherLxr-Alpha
dc.subject.otherIn-Vivo
dc.subject.otherG-Csf
dc.subject.otherGranulopoiesis
dc.subject.otherPhagocytosis
dc.subject.otherClearance
dc.subject.otherCells
dc.titleCoordinate regulation of neutrophil homeostasis by liver X receptors in mice
dc.typeinfo:eu-repo/semantics/Article
dc.typeArticle
dc.identifier.doi10.1172/JCI58393
dc.identifier.scopus84855427447
dc.identifier.isi000298769400036
dc.contributor.authorscopusid15755660400
dc.contributor.authorscopusid55403144300
dc.contributor.authorscopusid28567533000
dc.contributor.authorscopusid54884634800
dc.contributor.authorscopusid54883913900
dc.contributor.authorscopusid54884106700
dc.contributor.authorscopusid54884206300
dc.contributor.authorscopusid6603705291
dc.contributor.authorscopusid11539376600
dc.contributor.authorscopusid8527128700
dc.contributor.authorscopusid36727311700
dc.contributor.authorscopusid7402923672
dc.contributor.authorscopusid55445301000
dc.contributor.authorscopusid7007079890
dc.contributor.authorscopusid6602800046
dc.description.lastpage347
dc.description.firstpage337
dc.relation.volume122
dc.type2Artículo
dc.contributor.daisngid750105
dc.contributor.daisngid144719
dc.contributor.daisngid34354606
dc.contributor.daisngid11246376
dc.contributor.daisngid2471730
dc.contributor.daisngid29272277
dc.contributor.daisngid13100259
dc.contributor.daisngid179056
dc.contributor.daisngid1265296
dc.contributor.daisngid373513
dc.contributor.daisngid1257376
dc.contributor.daisngid5805401
dc.contributor.daisngid225640
dc.contributor.daisngid103250
dc.contributor.daisngid675311
dc.contributor.wosstandardWOS:Hong, C
dc.contributor.wosstandardWOS:Kidani, Y
dc.contributor.wosstandardWOS:A-Gonzalez, N
dc.contributor.wosstandardWOS:Phung, T
dc.contributor.wosstandardWOS:Ito, A
dc.contributor.wosstandardWOS:Rong, X
dc.contributor.wosstandardWOS:Ericson, K
dc.contributor.wosstandardWOS:Mikkola, H
dc.contributor.wosstandardWOS:Beaven, SW
dc.contributor.wosstandardWOS:Miller, LS
dc.contributor.wosstandardWOS:Shao, WH
dc.contributor.wosstandardWOS:Cohen, PL
dc.contributor.wosstandardWOS:Castrillo, A
dc.contributor.wosstandardWOS:Tontonoz, P
dc.contributor.wosstandardWOS:Bensinger, SJ
dc.date.coverdateEnero 2012
dc.identifier.ulpgces
dc.description.sjr8,963
dc.description.sjrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0002-2057-2159-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameCastrillo Viguera,Antonio Jesús-
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