Inflammasome Activation of IL-18 Results in Endothelial Progenitor Cell Dysfunction in Systemic Lupus Erythematosus.pdf

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1、InflammasomeActivationofIL-18ResultsinEndothelialProgenitorCellDysfunctioninSystemicLupusErythematosusThisinformationiscurrentasJ.MichelleKahlenberg,SethG.Thacker,CelineC.Berthier,ofJanuary4,2012ClemensD.Cohen,MatthiasKretzlerandMarianaJ.KaplanJImmunol2011

2、;187;6143-6156;Prepublishedonline4November2011;doi:10.4049/jimmunol.1101284http://www.jimmunol.org/content/187/11/6143DownloadedfromSupplementaryhttp://www.jimmunol.org/content/suppl/2011/11/04/jimmunol.11012Data84.DC1.htmlReferencesThisarticlecites52artic

3、les,27ofwhichcanbeaccessedfreeat:http://www.jimmunol.org/content/187/11/6143.full.html#ref-list-1www.jimmunol.orgSubscriptionsInformationaboutsubscribingtoTheJournalofImmunologyisonlineathttp://www.jimmunol.org/subscriptionsPermissionsSubmitcopyrightpermis

4、sionrequestsathttp://www.aai.org/ji/copyright.htmlEmailAlertsReceivefreeemail-alertswhennewarticlescitethisarticle.SignupatonJanuary4,2012http://www.jimmunol.org/etoc/subscriptions.shtml/TheJournalofImmunologyispublishedtwiceeachmonthbyTheAmericanAssociati

5、onofImmunologists,Inc.,9650RockvillePike,Bethesda,MD20814-3994.Copyright©2011byTheAmericanAssociationofImmunologists,Inc.Allrightsreserved.PrintISSN:0022-1767OnlineISSN:1550-6606.TheJournalofImmunologyInflammasomeActivationofIL-18ResultsinEndothelialProgeni

6、torCellDysfunctioninSystemicLupusErythematosus,1†‡J.MichelleKahlenberg,*SethG.Thacker,*CelineC.Berthier,ClemensD.Cohen,†MatthiasKretzler,andMarianaJ.Kaplan*Systemiclupuserythematosus(SLE)isanautoimmunediseasewithheterogeneousmanifestationsincludingsevereor

7、gandamageandvasculardysfunctionleadingtoprematureatherosclerosis.IFN-ahasbeenproposedtohaveanimportantroleinthedevelopmentoflupusandlupus-relatedcardiovasculardisease,partlybyrepressionofIL-1pathwaysleadingtoimpairmentsinvascularrepairinducedbyendothelialp

8、rogenitorcells(EPCs)andcirculatingangiogeniccells(CACs).Counterintuitively,SLEpatientsalsodisplaytranscriptionalupregulationoftheIL-1b/IL-18processingmachinery,theinflammasome.Tounderstandthisdichotomyanditsim