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1、Eur.J.Immunol.2007.37:1887–1904Immunomodulation1887ImmunomodulationImpairmentofdendriticcellfunctionbyexcretory-secretoryproducts:Apotentialmechanismfornematode-inducedimmunosuppressionMarielaSegura,ZhongSu,CiriacoPiccirilloandMaryM.StevensonCentrefortheStudyofHostResistance,ResearchIn
2、stituteoftheMcGillUniversityHealthCentre,McGillUniversity,Montreal,CanadaTodeterminewhetherhelminth-derivedproductsmodulatedendriticcell(DC)Received1/8/06function,weinvestigatedtheeffectsofexcretory-secretoryproducts(ES)andadultRevised18/3/07Accepted7/5/07wormhomogenate(AWH)derivedfrom
3、thegastrointestinalnematodeHeligmo-somoidespolygyrus(Hp)onmurinebonemarrow-derivedDC(BMDC).Comparedtothe[DOI10.1002/eji.200636553]TLR9ligandCpG,Hp-derivedproductsalonefailedtoinduceDCactivation.ES,butnotAWH,inhibitedBMDCcytokineandchemokineproductionandco-stimulatorymoleculeexpression(
4、CD40,CD86andMHCclassII)inducedbyTLRligation.TLRligand-independent,PMA-inducedDCactivationwasunaffectedbyES.RecipientsofES-treatedBMDCpulsedwithOVAhadsuppressedAbresponsesinvivo,irrespectiveoftheTh1orTh2isotypeaffiliation,comparedtorecipientsofcontrolOVA-pulsedBMDC.Importantly,suppressi
5、onoccurredeveninthepresenceofthepotenttype1adjuvantCpG.IncontrasttountreatedOVA-pulsedBMDC,ES-treatedBMDCpulsedwithOVA++–hadreducedco-stimulatorymoleculeandcytokineexpression.CD4CD25Foxp3Keywords:Tcells,whichsecretedhighIL-10levels,weregeneratedinco-culturesofOT-IIOVA-Adaptiveimmune+sp
6、ecificTCR-transgenicCD4TcellsandES-treatedBMDC.TheseIL-10-secretingresponses+TcellssuppressedeffectorCD4TcellproliferationandIFN-cproduction,thelatterDendriticcellseffectmediatedbyanIL-10-dependentmechanism.Together,theseresultsdemonstrateImmunomodulationthatnematodeESimpairedDCfunct
7、ionandsuppressedbothTh1andTh2adaptiveParasitic-helminthimmuneresponsespossiblybyinducingregulatoryTcells.TcellsIntroductionadvantageousinordertocompletetheirlifecyclethatsuchparasitesmaintainthesurvivalofthehostforasHelminthparasites,whichinduceahighlypolarizedlongaspossible,either
