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Flt3 Signaling-Dependent Dendritic Cells Protect against Atherosclerosis

DC FieldValueLanguage
dc.contributor.author박채규-
dc.date.accessioned2014-12-20T17:52:19Z-
dc.date.available2014-12-20T17:52:19Z-
dc.date.issued2011-
dc.identifier.issn1074-7613-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/95414-
dc.description.abstractEarly events in atherosclerosis occur in the aortic intima and involve monocytes that become macrophages. We looked for these cells in the steady state adult mouse aorta, and surprisingly, we found a dominance of dendritic cells (DCs) in the intima. In contrast to aortic adventitial macrophages, CD11c(+)MHC II(hi) DCs were poorly phagocytic but were immune stimulatory. DCs were of two types primarily: classical Flt3-Flt3L signaling-dependent, CD103(+)CD11b(-) DCs and macrophage-colony stimulating factor (M-CSF)-dependent, CD14(+)CD11b(+)DC-SIGN(+) monocyte-derived DCs. Both types expanded during atherosclerosis. By crossing Flt3(-/-) to Ldlr(-/-) atherosclerosis-prone mice, we developed a selective and marked deficiency of classical CD103(+) aortic DCs, and they were associated with exacerbated atherosclerosis without alterations in blood lipids. Concomitantly, the Flt3(-/-)Ldlr(-/-) mice had fewer Foxp3(+) Treg cells and increased inflammatory cytokine mRNAs in the aorta. Therefore, functional DCs are dominant in normal aortic intima and, in contrast to macrophages, CD103(+) classical DCs are associated with atherosclerosis protection.-
dc.description.statementOfResponsibilityopen-
dc.format.extent819~831-
dc.relation.isPartOfIMMUNITY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAntigens, CD/metabolism-
dc.subject.MESHAorta/drug effects-
dc.subject.MESHAorta/immunology-
dc.subject.MESHAtherosclerosis/genetics-
dc.subject.MESHAtherosclerosis/immunology*-
dc.subject.MESHAtherosclerosis/pathology-
dc.subject.MESHDendritic Cells/drug effects-
dc.subject.MESHDendritic Cells/immunology*-
dc.subject.MESHDendritic Cells/metabolism-
dc.subject.MESHGene Expression Regulation/immunology-
dc.subject.MESHLeukocyte Reduction Procedures-
dc.subject.MESHMacrophage Colony-Stimulating Factor/metabolism-
dc.subject.MESHMacrophages/immunology-
dc.subject.MESHMembrane Proteins/pharmacology-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Knockout-
dc.subject.MESHMonocytes/immunology-
dc.subject.MESHSignal Transduction*-
dc.subject.MESHfms-Like Tyrosine Kinase 3/genetics-
dc.subject.MESHfms-Like Tyrosine Kinase 3/metabolism*-
dc.titleFlt3 Signaling-Dependent Dendritic Cells Protect against Atherosclerosis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorJae-Hoon Choi-
dc.contributor.googleauthorCheolho Cheong-
dc.contributor.googleauthorDurga B. Dandamudi-
dc.contributor.googleauthorChae Gyu Park-
dc.contributor.googleauthorAnthony Rodriguez-
dc.contributor.googleauthorSaurabh Mehandru-
dc.contributor.googleauthorKlara Velinzon-
dc.contributor.googleauthorIn-Hyuk Jung-
dc.contributor.googleauthorJi-Young Yoo-
dc.contributor.googleauthorGoo Taeg Oh-
dc.contributor.googleauthorRalph M. Steinman-
dc.identifier.doi10.1016/j.immuni.2011.09.014-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01718-
dc.relation.journalcodeJ01034-
dc.identifier.eissn1097-4180-
dc.identifier.pmid22078798-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S1074761311004560-
dc.contributor.alternativeNamePark, Chae Gyu-
dc.contributor.affiliatedAuthorPark, Chae Gyu-
dc.rights.accessRightsnot free-
dc.citation.volume35-
dc.citation.number5-
dc.citation.startPage819-
dc.citation.endPage831-
dc.identifier.bibliographicCitationIMMUNITY, Vol.35(5) : 819-831, 2011-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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