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简介：ToscreenandidentifytheshortpeptideswithspecificbindingactivitytohumanCDS9andtodesigntheshort-peptideclampagainsttumorescape,thephagedisplaypeptidelibrarycontaining12peptideswasusedtoselectthehighlyexpressedspecificcoalescentpeptideofhumanCD59inCHOcells.Positivephageclonesobtainedafter5roundsofbiopanninganddetectedwithELISAwereobtained,inwhich8ofthemwithhighbindingactivitytohumanCD59weresequenced.The3sequencesthusobtainedshowedhighhomologywitheachandcertainhomologywithsequencewithhumanCD2(PubMed339HGAAENSISPSS),andallcontainedprimarystructureHXAXXXXXXPXX,ofwhichthissequencemaybethemimicconformationalepitopebindingtohumanCD59.Theseresultsinthepresentstudymaybehelpfultodesigntheshort-peptideclampagainsttheactivesitesofCD59ontumorescape.

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简介：ToexploretheeffectofrhlL-15onCB-CD34^+stemcellscommittingtoNKcells,CD34^+stemcellswereobtainedfromcordblood(CB)bymagnetic-assistedcellsorting(MACS)method.CD3,CD16andCD56moleculesexpressedoncellsurfaceweredetectedbyflowcytometer.MTFmethodwasusedtotestthecytotoxicityofNKcells.Theresultswerethatstemcellfactor(SCF)alonehasnoeffectonCD34^+stemcells.IL-15stimulatedCD34^+stemcellscommittoNKcells,andSCFshowedstrongsynergisticeffectwithIL-15.ItwasconcludedthatIL-15andSCFplayeddifferentrolesduringNKcelldevelopment,llr15promotedCD34^+stemcellsdifferentiatetoNKcellprecursorandSCFimprovedtheeffectsofIL-15onNKcelldifferentiation.

简介：Twenty-oneyearsaftermalariaantigenswerefirstclonedavaccinestillappearstobealongwayoff.Therehavebeenperiodsofgreatexcitementandinmodelsystemssubunitvaccinehomologuescaninducerobustprotection.However,significantchallengesexistconcerningantigenicvariationandpolymorphism,immunologicalnon-respons-ivenesstoindividualvaccineantigens,parasite-inducedapoptosisofimmuneeffectorandmemorycellsandimmunedeviationasaresultofmaternalimmtmityandalterationsofdendriticcellfunction.

简介：TostudythemechanismofinfectionofEpstein-Barrvirus(EBV)ingastriccarcinomacells,theAkataandP3HR-1strainsofEBVwereusedastheteststrainsofviruses,andthesignetringcelllineHSC-39ofgastriccarcinomacellswasusedasthetargetcellsofinfection.Thevirus-infectedcellcloneswereisolatedbylimiteddilutionmethod.ItwasfoundthattheEBV-encodedsmallRNA(EBER)couldbedetectedintheinfectedcells.TheAkataandP3HR-1EBVinfectedparentalcellsandmostofclonesexpressedEBNA1,butnotEBNA2.Latentmembraneprotein(LMP-1)andLMP-2,andtheQpromoter(p),butnottheCp/WpforEBNAgenetranscriptionwasactiveintheinfectedparentalcellsaswellasalltheclones.UninfectedHSC-39cellsdidnotexpressCD21,however,AkatabutnotP3HR-1EBV-infectedclonesex-pressedlowlevelofCD21mRNA.TheseresultsdemonstratethatHSC-39cellsaresusceptibletobothEBVstrainsandEBVinfectsHSC-39cellsthroughtheCD21-independentpathway.ThisstudydefinesasignetringtypeofgastriccarcinomacellslineasauniquetargetcellsforthestudyofEBVinfectionmechanism.

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简介：Inthepresentstudy,theeffectofblockageofthecostimulatorysignalCD86attimeofimplantationontheexpressionsofTGF-β1,MMP-9,TIMP-3andPAI-1proteinsatthematernal-fetalinterfaceandtheoutcomeofpregnancyinmurineabortion-pronemodelwasinvestigated,inwhichtheCBA/JxDBA/2matingswereusedastheabortion-pronemodelandtheCBA/J×BALB/cmatingsusedasthenormalpregnantmodel.Thestudywasperformedinfollowingthreegroups:2groupsoftheabortion-pronemodel,whichwereexperimentalgroupandcontrolexperimentalgroup,and1groupofnormalpregnantmodel,andeachgrouphad10pregnantCBA/Jmiceexclusively.FemalepregnantCBA/Jmiceintheexperimentalgroupreceivedanintraperitoneal(i.p.)injectionof100μgofantimouseCD86mAbin200μlofPBSatday4.5ofgestation,andtheirrelevant-isotopematchedratIgG2bwasadministratedinthecontrolexperimentalgroupwiththesamedosageandatsametime.Forthenormalpregnantgroup,notreatmentwasgiven.ThepregnantCBA/Jmicewerekilledonday13.5ofgestation.Then,theembryoresorptionratewascalculatedandtheexpressionsofTGF-β1,MMP-9,TIMP3andPAI-1weredetectedbyusingimmunohistochemicalmethods.Itwasdemonstratedthattheembryoresorptionrateintheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(x2=7.441,P=0.006),buttherewasnosignificantdifferencewiththatinnormalpregnantgroup(x2=0.016,P=0.898).TheexpressionsofTGF-β1andPAI-1intheexperimentalgroupweresignificantlyincreasedincomparisonwiththatinthecontrolexperimentalgroup(P=0.010,P=0.003,respectively),withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).However,theexpressionofMMP-9intheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(P=0.012)withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).Theexpression

简介：ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.