简介:目的探讨在ConA诱导肝细胞损伤过程中的Fas抗原的表达情况以及CsA干预对其损伤的影响。方法尾静脉注射ConA(20mg·kg^-1)于BALB/c小鼠作为试验组;提前半小时予以CsA(25mg·kg^-1)后再按试验组处理作为CsA组。观察血清中ALT、AST含量动态变化及肝组织细胞Fas抗原表达。结果试验组血清中ALT、AST进行性升高,在12h时与对照组、CsA组比较均P<0.01。试验组有大量Fas抗原表达的肝细胞,且数量逐渐增多、信号逐步增强。对照组和CsA组血清中ALT、AST变化不大,肝细胞Fas抗原表达不明显。结论Fas配体-抗原系统介导了ConA所致肝损伤,细胞毒性T淋巴细胞的激活是其肝细胞损伤的重要机理。
简介:ObjectivesToinvestigatetheassociationofsolubleFasligand(sFasL)andsolubleFasreceptor(sFas)withhumanchroniccongestiveheartfailure(CHF).MethodsTheserumlevelofsFasLandsFasin33patientswithCHF(13incardiacfunctionclassⅡ,17inclassⅢ,3inclassⅣ,NYHA)wasassessedwithenzyme-linkedimmunosorbentassay,andwascomparedwiththatof18age-,bloodpressure-matchedpatientswithcardiacfunctionclassⅠ(NYHA).ResultsTherewasnodifferenceinthelevelofsFasLbetweenthetwogroups[CHFgroup:231.50+/-84.50(cardiacfunctionclassⅡ216.50+/-96.00,classⅢ226.80+/-85.70,classⅣ244.00+/-73.00)vs.cardiacfunctionclassIgroup:217.50+/-89.00pg/mL,P>0.05].However,thelevelofsFaswassignificantlyhigherinthepatientswithCHFthanthoseofcardiacfunctionclassIgroup[CHFgroup:1353.30+/-507.71(cardiacfunctionclassⅡ1154.85+/-371.20,classⅢ1412.88+/-493.62,classⅣ1875.67+/-806.
简介:目的:探讨MMP-9、CD44vs和Fas抗原表达与非小细胞肺癌(NSCLC)侵袭转移的关系。方法:采用免疫组织化学SP法分别检测MMP-9、CD44vs和Fas抗原在83例NSCLC组织中的表达。结果:83例NSCLC组织中MMP-9表达40例(48.19%)CD44v6表达51例(61.45%),Fas抗原表达47例(56.63%),MMP-9和CD44vs共同表达40例(48.19%)。MMP-9、CD44vs和Fas抗原表达与临床分期、淋巴结转移明显相关(P<0.05);而与患者年龄、性别、病理类型无关(P>0.05)。MMP-9、CD44vs表达有随组织分化程度降低呈增高趋势,而Fas抗原表达则呈降低趋势。单因素分析表明MMP-9、CD44v6阳性表达者的平均生存期较阴性者短,Fas抗原阳性表达者的平均生存期较阴性者长。Cox回归分析表达MMP-9、CD44v6表达与患者的生存率有关,Fas抗原对患者有保护趋势。结论:MMP-9、CD44vs和Fas抗原等多种因素在NSCLC侵袭、转移中起重要作用。其中CD44v6的作用最为重要。
简介:<正>Fasligand(FasL)wasfirstdescribedfunctionallyasaninduciblecellsurfacemoleculeusedbycytotoxicTcellstoinduceapoptoticcelldeathintumorcellsandactivatedlymphocytes.WiththeidentificationofFasastheIprgeneproduct,FasLbecamerecognizedasamoleculeinvolvedindown-regulationoftheimmunesystem.WhileFasLcanbeusedtoefficientlykillFas-expressingtumorcellsaswellasactivatedTandBlymphocytesinvitro,attemptstouseFasLtherapeuticallytotreatcancerortopreventtransplant
简介:ApoptosisproducedinBcellsthroughFas(APO-1,CD95)triggeringisregulatedbysignalsderivedfromothersurfacereceptors:CD40engagementproducesupregulationofFasexpressionandmarkedsusceptibilitytoFas-inducedcelldeath,whereasantigenreceptorengagement,orIL-4Rengagement,inhibitsFaskillingandinsodoinginducesastateofFas-resistance,eveninotherwisesensitive,CD40-stimulatedtargets.SurfaceimmunoglobulinandIL-4RutilizeatleastpartiallydistinctpathwaystoproduceFas-resistancethatdifferentiallydependonPKCandSTAT6,respectively.Further,surfaceimmunoglobulinsignalingforinducibleFas-resistancebypassesBtk,requiresNF-κB,andentailsnewmacromolecularsynthesis.TerminaleffectorsofBcellFas-resistanceincludetheknownanti-apoptoticgeneproducts,Bcl-XLandFLIP,andanovelanti-apoptoticgenethatencodesFAIM(FasApoptosisInhibitoryMolecule).faimwasidentifiedbydifferentialdisplayandexistsintwoalternativelysplicedforms;faim-Sisbroadlyexpressed,butfaim-Lexpressionistissue-specific.TheFAIMsequenceishighlyevolutionarilyconserved,suggestinganimportantroleforthismoleculethroughoutphylogeny.InducibleresistancetoFaskillingishypothesizedtoprotectforeignantigen-specificBcellsduringpotentiallyhazardousinteractionswithFasL-bearingTcells,whereasautoreactiveBcellsfailtobecomeFas-resistantandaredeletedviaFas-dependentcytotoxicity.InadvertentoraberrantacquisitionofFas-resistancemaypermitautoreactiveBcellstoescapeFasdeletion,andmalignantlymphocytestoimpedeanti-tumorimmunity.
简介:<正>ThesusceptibilityofprimaryBcellstoFas(APO-1,CD95)-mediatedapoptosisisregulatedbysignalsderivedfromadditionalsurfacereceptors.CD40engagementproducesupregulationofFasexpressionandinducesmarkedsensitivitytoFas-inducedcelldeath,whereasBcellantigenreceptor(BCR)engagementinhibitsFaskillingandtherebyproducesFas-resistance,eveninotherwisesusceptible,CD40-stimulatedtargets.BCRsignalingforinducibleFas-resistancedevelopsoveraperiodof12hoursanddependson
简介:IncreasedexpressionofFasbyhematopoieticprogenitorsinaplasticanemia(AA)suggeststhatFas/Fasligand(FasL)systemplaysakeyroleintheformationofseverepancytopenia.Tofurtherconfirmtheabovehypothesis,Tcellsfrom8patientswithAAweresystematicallystudiedfortheirFasL'sdistributionpattern,releasingmannerandproapoptoticactivity,comparedwithnormalrestingTcellsandartificiallyactivatedTcellblasts.TheresultsdemonstratedthatAATcellsabnormallyexpressedlowlevelsofmembrane-boundFasLandcontainedhighlevelsofintracellularFasLwhichcouldbetriggeredtoreleasebyhigh-dosephytohemagglutinin(PHA)pulse-stimulation.ThesupernatantsfromthePHA-stimulatedAATcellshadapparentcytotoxicityagainstFasL-sensitiveJurkatcells,whichcouldbesignificantlyinhibitedbymonoclonalantibodyagainstFasLinadose-dependentmanner,ornearlycompletelyabrogatedbyultracentrifugation.TheabovephenomenaalsoappearedonartificiallyactivatedTcellblasts,butthiswasnotthecaseonnormalrestingTcells.TheseresultsindicatethatAATcellisatypeof'preactivated'Tlymphocyte,characterizedbyoverexpressionofFasL,especiallyintracellularFasLwhichcanbestimulatedtoreleaseinbioavtiveexosomesboundform.Takentogether,ourdataprovidefurtheranddirectevidenceforthehypothesisthatTcellsmightmediatethedestructionofhematopieticprogenitorinAAthroughFas/FasLsystem.
简介:摘要目的探讨血清CA125在临床中的应用,特别是在卵巢癌诊断中的最要性.方法化学发光法.结论卵巢癌和宫颈癌中CA125会有不同程度的增高.结论子宫内膜异位症、宫颈癌、肺癌等是引起CA125增高的可能原因.卵巢癌对CA125较为敏感,对卵巢癌的的诊断有极大的临床意义.关键词卵巢癌;子宫内膜异位症;宫颈癌;肺癌;CA125中图分类号R737.3文献标识码B文章编号1001-5302(2015)09-0782-02