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.
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简介:ToobservetheeffectofGardeniaextractZGontheadsorptionquantityofherpessimplexvirustype1(HSV-1)soastoexplorethemechanismofitsantiviralactivity,fluoresceinisothiocyanate(FITC)wasusedasthefluorescentprobetolabelvirusesandheparinsodiumwasusedascontrol.Meanwhile,theeffectofGardeniaextractZGontheadsorptionquantityonthesurfaceofHep-2cellswasdeterminedbyflowcytometry.ItwasdemonstratedthatadsorptionofHSV-1onthesurfaceofHep-2cellsexhibitedthecharacterofsaturationandspecificityandheparinsodiumcouldpreventattachmentofvirusesonthesecells.Theseresultsareinaccordwiththosereportedpreviously.Itwasalsoprovedthatthemannerofdrug-usepriortoadsorptionorsimultaneoususeofdrugandadsorptionwasbetterthanadsorptionpriortodrug-use,andtheinhibitionratesoftheformerandlattermannerwere84.76%and82.92%respectively.Threemannersofdrug-usewithGardeniaextractZGwerealleffectivetoreducetheadsorptionquantityofviruses,especiallythemannerofsimultaneoususeofdrugandadsorptionwithanadsorptioninhibitionrateof68.46%.Fromtheaboveobservation,itisapparentthatthemechanismofanti-viralactivityofGardeniaextractZGmaybeviaseveralstepsinvolvedintheHSV-1adsorption.
简介:WeareracingwithHIV-1,theetiologicagentforAIDSinhumanbeings[1,2],withtwopossibleendconsequences:ifwewin,HIV-1willbeunderourcontrolbyimmunologicortherapeuticmeasures;ifHIV-1wins,theSIVAfricanmonkeys'storywouldrepeatinhumans,i.e.,onlythefewindividualsthatarenotkilledbythevirus
简介:Wehavepreviouslydemonstratedtheabilityofmalariaparasitestointerferewithspecificimmuneresponses.CD4Tcellsspecifictoparasiteantigens,butnotCD4Tcellsspecifictoanirrelevantantigen,ovalbumin(OVA),aredeletedviaapoptosisduringmalariainfection.Itisofinterest,therefore,toinvestigatetheimmuneresponsesthatdevelopedfollowingvaccinationwiththe19kDacarboxylterminusofthemerozoitesurfaceprotein1(MSP119)inmicethathadpreviouslyexperiencedmalariainfection.Inthisstudy,pre-exposureofmicetoPlasmodiumyoeliielicitednativeanti-MSP119antibodyresponses,whichcouldbeboostedbyvaccinationwithrecombinantMSP119,Likewise,infectionofMSP119-primedmicewithPlasmodiumyoelii(P.yoelii)ledtoanincreaseofanti-MSP119antibodies.MSP119vaccinationofmalariapreexposedmiceorimmunizationbyinfection/cureofMSP119-primedmiceenabledthemicetosurvivechallengeinfection,withtheformergrouphavingslightlylowerparasitaemia.Thedatasuggestthatexposuretomalariainfectionprimesanaturalimmuneresponsewhichcanbeboostedbyvaccination.Thisinformationisrelevanttothedevelopmentofavaccineforuseinindividualslivinginmalaria-endemicareas.
简介:ToexplorethemechanismoftheinhibitionofHIV-1byMycoplasmafermerttans,culturesupernatantsandthallodicproteinsfromM.fermerttansPG18werepreparedandtheproteincomponentsofthesupernatantswerepurifiedwithhighperformanceliquidchromatography(HPLC).Theinhibitoryactivitiestoreversetranscriptase(RT)andthenucleaseactivitiesweredetected;theinfluenceofM.fermerttansonIL-10secretionbybothnormalandH1V-1infectedhumanPBMCweredetermined,andtheinhibitoryeffectofrhIL-10onH1V-1replicationwasdetectedwithEI,ISAmethod.Theresultsshowedthatthepurifiedproteinswithamolecularweightof67-100kDaor10-25kDashoweda36%or34%inhibitoryac-tivitytoRTandpartialnucleaseactivity.ThethallodicproteincouldinducebothnormalandH1V-1infectedPBMCtosecretIL-10remarkably,andtothelatter,thiseffectwasmoreapparent.WhilerhIL-10couldinhibitreplicationofH1V-1inPB-MCinvitroinadose-dependantmanner.ItconcludesthattheinhibitoryeffectoftheM.fermentansPG18culturesupernatantsonRTandthepromotingeffectofPG18thallodicproteinonIL-10secretioninPBMCexplainthemechanismsofinhibitiontoHIV-1byM.fermentansPG18.