MFG-E8 Regulates the Immunogenic Potential of Dendritic Cells Primed with Necrotic Cell-Mediated Inflammatory Signals 英文参考文献.docVIP

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MFG-E8 Regulates the Immunogenic Potential of Dendritic Cells Primed with Necrotic Cell-Mediated Inflammatory Signals 英文参考文献.doc

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MFG-E8 Regulates the Immunogenic Potential of Dendritic Cells Primed with Necrotic Cell-Mediated Inflammatory Signals 英文参考文献

MFG-E8RegulatestheImmunogenicPotentialof DendriticCellsPrimedwithNecroticCell-Mediated InflammatorySignals MuhammadBaghdadi,ShigekiChiba,TsunakiYamashina,HironoriYoshiyama,MasahisaJinushi* ResearchCenterforInfection-AssociatedCancer,InstituteforGeneticMedicine,HokkaidoUniversity,Sapporo,Japan Abstract Dendriticcells(DC)manipulatetissuehomeostasisbyrecognizingdyingcellsandcontrollingimmunefunctions.However, the precise mechanisms by which DC recognize different types of dying cells and devise distinct immunologic consequencesremainlargelyobscure.Herein,wedemonstratethatMilk-fatglobule-EGFVIII(MFG-E8)isacriticalmediator controllingDCimmunogenicityininflammatorymicroenvironments.MFG-E8restrainsDC-mediateduptakeandrecognition ofnecroticcells.TheMFG-E8-mediatedsuppressionofnecroticcelluptakebyDCresultedinthedecreasedproinflammatory cytokinesproductionandactivatedsignalcomponentssuchasSTAT3andA20,whicharecriticaltomaintaintolerogenic properties of DC. Furthermore, the DC-derived MFG-E8 negatively regulates the cross-priming and effector functions of antigen-specificTcellsuponrecognitionofnecroticcells.MFG-E8deficiencyenhancesanabilityofnecroticcell-primedDC to stimulate antitumor immune responses against established tumors. Our findings define what we believe to a novel mechanismwherebyMFG-E8regulatestheimmunogenicityofDCbymodulatingthemodesofrecognitionofdyingcells. ManipulatingMFG-E8levelsinDCmayserveasausefulstrategyforcontrollinginflammatorymicroenvironmentscausedby variouspathologicalconditionsincludingcancerandautoimmunity. Citation:BaghdadiM,ChibaS,YamashinaT,YoshiyamaH,JinushiM(2012)MFG-E8RegulatestheImmunogenicPotentialofDendriticCellsPrimedwithNecrotic Cell-MediatedInflammatorySignals.PLoSONE7(6):e39607.doi:10.1371/journal.pone.0039607 Editor:AllenWaziri,UniversityofColoradoSchoolofMedicine,UnitedStatesofAmerica ReceivedFebruary21,2012;AcceptedMay23,2012;PublishedJune25,2012 Copyright: ? 2012 Baghdadi et al. This is an open-access article distributed under th