简介：ToinvestigatetheimbalancestateofhelperTlymphocytes(Th)andcytotoxicTlympho-cytes(Tc)andtherolesofTh1/Th2/Th3andTc1/Tc2cellsinrenaltransplantationrejection,theper-centagesofthesecellsinperipheralbloodof24casesofrenaltransplantationrecipientswithacutere-jectionandthedynamicchangesoftheCD4/CD8ratioweredeterminedbyflowcytometryanalysis,while30casesofhealthyindividualsweresetupascontrols.Inthesehealthycontrols,thepercentagesoftheTh1,Th2andTh3cellswere(10.45±8.15)%,(5.05±4.15)%and(3.90±3.21)%,andthoseofTc1andTc2cellswere(9.83±7.03)%and(4.51±2.17)%,respectively.However,thepercentagesofTh1andTclcellsinperipheralbloodofthestablerecipientsaftertransplantationwere(7.29±5.62)%and(7.04±5.15)%,showingdefinitereduction,whilethoseofTh2,Th3andTc2cellsshowedsignificantincrease,(6.34±5.67)%,(4.94±4.14)%and(6.86±4.42)%,respectively.Incaseofrecipientswithacuterejection,thepercentagesofTh1andTc1cellsappearedtobe(18.55±13.21)%and(15.84±11.72)%,alsoshowingsignificantincrease,butthoseofTh2,Th3andTc2cellsappearedtobereduced,(4.19±3.62)%,(3.02±2.83)%and(3.88±1.63)%,respectively.Significantdifferencescouldbedetectedamongthesethreegroups(P<0.05).TheCD4/CD8ratioincaseswithacuterejectionwashigherthanthoseofstablerecipients(2.24±0.59vs1.95±0.45),butthatofthestablerecipientsandhealthycontrols(1.98±0.31)showednoanysignificantdifference.Fromtheaboveobservation,itisevidentthatimbalancebetweenTh1,Th2andTh3withTc1andTc2cellsmayexistafterrenaltransplantationandprobably,theim-muneimbalancemaybeinducedthroughthesecretionofcytokinesINF-γbyTh1orTc1cells,Ⅱ-4byTh2andTc2cellsandTGF-βbyTh3.

简介：ApoptosisplaysanessentialroleinTcellbiology.ThymocytesexpressingnonfunctionalorautoreactiveTCRsareeliminatedbyapoptosisduringdevelopment.ApoptosisalsoleadstothedeletionofexpandedeffectorTcellsduringimmuneresponses.Thedysregulationofapoptosisintheimmunesystemresultsinautoimmunity,tumorogenesisandimmunodeficiency.Twomajorpathwaysleadtoapoptosis:theintrinsiccelldeathpathwaycontrolledbyBcl-2familymembersandtheextrinsiccelldeathpathwaycontrolledbydeathreceptorsignaling.Thesetwopathwaysworktogethertoregu

简介：Uponencounteringtheantigen(Ag),theimmunesystemcaneitherdevelopaspecificimmuneresponseofenteraspecificstateofunresponsiveness,tolerance.TheresponseofBcellstotheirspecificAgcanbeactivationandproliferation,leadingtotheimmuneresponse,oranergyandactivation-inducedcelldeath(AICD),leadingtotolerance.AICDinBlymphocytesisahighlyregulatedeventinitiatedbycrosslinkingoftheBcellreceptor(BCR).BCRengagementinitiatesseveralsignalingeventssuchasactivationofPLCγ,Ras,andPI3K,whichgenerallyspeaking,leadtosurvival.However,intheabsenceofsurvivalsignals(CD40orIL-4Rengagement),BCRcrosslinkingcanalsopromoteapoptoticsignaltransductionpathwayssuchasactivationofeffectorcaspases,expressionofpro-apoptoticgenes,andinhibitionofpro-survivalgenes.ThecomplexinterplaybetweensurvivalanddeathsignalsdeterminestheBcellfateand,consequently,theimmuneresponse.

简介：<正>ThesusceptibilityofprimaryBcellstoFas(APO-1,CD95)-mediatedapoptosisisregulatedbysignalsderivedfromadditionalsurfacereceptors.CD40engagementproducesupregulationofFasexpressionandinducesmarkedsensitivitytoFas-inducedcelldeath,whereasBcellantigenreceptor(BCR)engagementinhibitsFaskillingandtherebyproducesFas-resistance,eveninotherwisesusceptible,CD40-stimulatedtargets.BCRsignalingforinducibleFas-resistancedevelopsoveraperiodof12hoursanddependson

简介：Immunotherapythatspecificallytargetstumorcellsisthepreferredapproachtoinducetumorregression.Overthepastdecade,significantprogresshasbeenmadeindevisingvariousmethodstodirecttheimmunesystemtorespondtotumorcells.Themajorhurdleforsuccessfulimmunotherapyistoovercomeimmunetoleranceinthetumormicroenvironment.Recentclinicaltrialswithdendriticcell-basedvaccination[1,2]andCTLA4blockingantibodies[3]haveshowngreatpromise,thoughcompletecancerregressionisnotalwaysachieved[4].Currently,alternativestrategiespotentiallyleadingtocancereradicationorregressioninanimalorclinicalmodelsarebeingenthusiasticallypursued.InthisissueofCellResearch,Wangetal.reportanovelwaytoinducetumorimmunitybytheuseofirradiatedautologousTcells[5].

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：TheimmunomodulationofseveralChargedsyntheticpolymerscontainingphosphorusinthebackbonewasstudiedinvitrothroughexaminingtheirinhibitionorpromotioneffectontheproliferatioinofbothTandBlymphocytes,Itisfoundthatpolymersbasedonlongchainalkylesteroftyrosineexhibitimmunomodulativeactivity.NegativelychargedpolymersshowstimulativeactivityonLPS-inducedBlymphocytesproliferation.PositivelychargedpolymersexhibitinhibitoryactivityonbothConA-inducedTlymphocytesandLPS-inducedBlymplhyocytesproliferation.

简介：ObjectiveToestablishalymphocytelinecapableoflongsurvivalandexpressinghumanNT-3tolayafoundationforfutureanimalandhumancochleargenetransfectionresearch.MethodsWecollectedlymphocytesfromnormalhumanbloodviaFicollfluidandaddedIL-2intotheserumculturemediumtopromotelymphocytegrowth.TheNT3cDNAwasobtainedbyRT-PCRandligatedwiththeeukaryonvectorwhichispIRES-DsRed2usingT4DNAenzyme.TheNT3cDNAgenewastransfectedintothelymphocytelineusingcationicliposome(LP2000).ThelymphocytestransfectedwithNT3-cDNAwereexaminedbyRT-PCRandWestern-blotmethods.ResultsWeestablishedanewmethodtoextendinvitrolymphocytessurvivaltimeandtotransfectNT3intolymphocytes.Thegeneticallyengineeredlymphocyteswerecapableofsurvivingoverrelativelylongtime.PositiveproteinsignalswereobtainedbyWesternblot.ConclusionsUsinglymphocytesastheintermediary,recombinedplasmidpIRES-DsRed2NT3isusedtoestablishalymphocytelinethatexpressesandsecretesNT3.Thiscelllinecanbeusedinfutureanimalgenecochleartransfectionresearchandmayhelpfindanintermediarycelllineforgenetherapyforhumandeafness.

简介：Recombinanthumanprolactin(rhPRL)wasadministeredtohuPBL-SCIDmicetodetermineitseffectsonhumanimmunologicreconsfitutionandfunction.ThehuPBL-SCIDmiceweregiven10μgI.p.InjectionofrhPRLeveryotherdayforatotalof10injectionsafterhuPBLweretransferred.TheresultsdemonstratedthatrhPRLimprovedtheengraftmentoflymphocytesintothymus,lymphnodesandspleens,showingthatthecellularitiesoftheseorgansincreasedalthoughthecellularitiestendedtovarydependingonthedonor.TheamountsofhumanTcells(HLA-ABC+/CD3+)increasedgreatlyinthymus(14.2folds),spleen(4.16folds)andlymphnodes(40.18folds)afterrhPRLinjections.TheamountsofhumanBcells(HLA-ABC+/CD19+)alsoincreasedgreatlyinlymphnodes(42.5folds)andspleen(5.78folds).ThelymphnodecellsfromtherhPRL-treatedhuPBL-SCIDmiceweremoresensitivetoPHAstimulation([3H]thymidineincorporation).ThesupernatantofPHA-stimulatedPBLfromrhPRL-treatedhuPBL/SCIDchimerismcontainedmorecytokines(IFN-γandIL-2).Thenaturalcytotoxicityagainsthumansensitivetargetcells,K562cells,fromspleenandbonemarrowofhPBL/SCIDchimerismwassignificantlyenhancedbyrhPRLadministration.ThelymphnodecellswerestimulatedwithLPSinvitrofor3daysandthelymphocytesfromtherhPRL-treatedhuPBL-SCIDmiceweremoresensitivetomitogenstimulation.BothserumtotalIgGlevelandIgMlevelofrhPRL-treatedhuPBL/SCIDchimerismwereincreased,andevenwithoutDT-rechallengethebaselineofDT-specificIgGwaselevatedafterrhPRLtreatmentinhuPBL-SCIDmice.Thus,rhPRLstimulationpromotesreconstitutionofhumanimmunesysteminhuPBL-SCIDmice.

简介：TheaimofthisstudyistoelucidatethemolecularandcellularmechanismsunderlyingtheimmunosuppressiveeffectofSanchiextract(SE)viainvestigatingtheeffectsofSEontheactivationandproliferationofmurinelymphocytesandNOsecretionbyperitonealmacrophagesinvitro.ConAwasusedtoactivatelymphocytes,andexpressionofCD69onTcellsandCFSElabeledcelldivisionweredetectedbyflowcytometry.MurineperitonealmacrophageswerestimulatedwithLPSorlymphocytesculturesupemate(LCS)andtheconcentrationofNOwasdeterminedbyGriessreagentassay.After6hofculture,SErangingfrom50to100μg/mldownregulatedCD69expressiononConA-activatedTcells,whileSErangingfrom12.5to100μg/mlinhibitedtheproliferativeresponseoflymphocytestoConA.Additionally,SE(12.5-100μg/ml)inhibitedsecretionofNObyperitonealmacrophagesstimu-latedbyLPSorLCS.ThisstudyrevealsthatSEinhibitstheactivationandproliferationofmurinelym-phocytesandNOsecretionbyperitonealmacrophages.

简介：Fas/CD95表面受体调停各种各样的房间的快速的死亡打字，包括有为触发autoimmunity的潜力的autoreactiveT房间。这里，我们表明那的船边交货的现在的新奇方面定义一种“社会”的尺寸到导致受体的apoptosis。船边交货刺激很快导致在附近的T房间之间的广泛的膜nanotube形成。这极其依赖于RhoGTPases然而并非在caspase激活上。包括活跃caspases的膜和cytosolic元素的双向转移能被观察经由这些nanotubes发生。Nanotube形成和死亡信号的细胞间的交换在从有在船边交货受体的自体免疫的lymphoproliferative症候群harbouring变化的病人的T淋巴细胞是有缺点的。我们断定调停nanotube的交换组成扩充在附近的T房间之间发信号的死亡的繁殖的细胞间的通讯的一种新奇形式。

简介：Objective:ThisstudyanalyzedtheTlymphocytesandThl/Th2typecytokineprofileshiftintheperipheralbloodofpatientswithrecurrentgenitalherpes(RGH).Methods:Immunofluorescentstainingofcellsurfaceantigenandintracellularcytokines(IL-2,IL-4,IL-12,IFN-r)inperipheralbloodfrom20RGHpatientsand10controlswereanalyzedusingflowcytometrictechniques.Results:RGHpatientshadsignificantlylowerlevelsofCD3^+Tcells,CD4^+TcellsandCD4^+T/CD8^+Tcellsratiocomparedtocontrollevels(P<0.001),andIL-2-producing,IFN-r-producingandIL-12-producingTcellswereincreasedinRGHpatients(CD4^+T:P<0.001,CD8^+T:P<0.05respectively),whereasIL-4-producingTcellswereincreasedinRGHpatientscomparedtocontrols(CD4+T:P<0.05;CDS^+T:P<0.001respectively).Conclusions:RGHpatientshaveTlymphocytesubsetvariationsandThl/Th2cytokinechanges.TheincreaseinTh2cellsThl/Th2imbalancemayhaveimportantimplicationsforRGHpathogenesis.

简介：到真菌的促进感受性经常导致是特别地困难的临床上设法的气喘的一种严重形式，导致在这些病人的增加的病态和住院。尽管B淋巴细胞可能通过IgE的生产加重气喘症状，这些房间可能也在对吸入的真菌的保护的反应是重要的。通过cytokine版本和T房间相互作用，这些淋巴细胞可能也影响航线墙纤维变性的发展和维护。JH−/−老鼠为抗体的重链部件缺乏JH基因，它为B房间功能和幸存是批评的。这些动物在很多有免疫力的回答便于B淋巴细胞的角色的说明；然而，JH−/−老鼠没被用来学习真菌的过敏症。在这研究，我们用曲霉属菌fumigatus检验了B淋巴细胞的角色模仿被环境真菌的暴露触发的人的航线疾病的鼠科的真菌的高空过敏症模型。我们在敏化的野类型的BALB/c和J暴露于的H−/−老鼠重复了真菌的暴露并且没在大航线附近在航线hyperresponsiveness，全面肺的发炎或骨胶原免职发现差别。然而，Th2类型cytokinesIL-4和IL-13的层次显著地在J相对BALB/c控制的H−/−鼠标。由对比，煽动性的cytokinesIL-17A和IL-6的层次显著地在JH−/−动物，并且有显著地更柔韧的航线嗜曙红血球过多和neutrophilia比在控制动物。一起拿，这些调查结果表明淋巴细胞帮助在肺的分隔空间调整granulocytic回答到真菌的暴露的那B。

简介：Interleukin-15(IL-15)为记忆CD8+和CD4+T的幸存是必要的房间子集，和天赋漂亮、自然的漂亮T房间。这里，我们描述一迄今在调整天真的CD4+T房间的homoeostasis的IL-15的unreported角色。从非肥胖的糖尿病患者(点头)的splenocytes的采纳转移在在lymphopenicNOD.scid.Il15−/−老鼠的T房间的增加的homeostatic扩大的老鼠结果什么时候与NOD.scid接受者相比。CD4+T房间的增加的累积也在NOD.Il15−/−老鼠被观察，显示那条IL-15-dependent规定也当淋巴球减少症不在时发生。缺乏IL-15Rα的NOD.scid老鼠；锁住，然而并非缺乏普通gamma的那些也锁住表演CD4+T房间的增加的累积。这些调查结果显示IL-15-mediated规定在CD4+T房间上直接发生并且要求IL-15的trans演讲。当IL-15不在时膨胀发信号的CD4+T房间不获得古典规章的T房间的特征。更确切地说，当IL-15表演不在时膨胀的CD4+T房间损害了导致抗原的激活和IFN-γ；生产。把调查结果基于这些，我们建议天真的CD4+T房间分隔空间的IL-15-dependent规定可以代表控制的另外的层潜在地阻挠逃离中央忍耐的autoreactive房间，当允许记忆T房间的扩大时。

简介：决定区域3的补充(CDR3)的分析一些由immunoscopespectratyping技术的T淋巴细胞受体(TCR)成功地被使用了在自体免疫的疾病和感染疾病调查TCR的差异。在这研究，我们由immunoscopespectratyping技术在四个正常志愿者的人的外部血淋巴细胞为所有32个TCRAV基因家庭调查了CDR3长度分发的模式。PCR产品在1.5%agarose胶化电气泳动上展出了一个卑微的乐队，这被发现。每个TCRAV家庭在6%上展出了超过8个乐队定序胶化电气泳动。所有TCRAV家庭的CDR3spectratyping与不同CDR3长度显示出标准Gaussian分布，并且CDR3的表示频率在基因家庭之中是类似的。大多数在TCRAV家庭的CDR3在框架重新结合。然而，一些CDR3显示出外面框架基因重新整理。另外，我们发现在一些TCRAV家庭，在最长的CDR3和最短的CDR3之间有18氨基酸差异。这些结果可能是有用的进一步在健康人和疾病状态学习人的TCR基因，TCRCDR3基因全部剧目，和全部剧目飘移的再结合机制。

简介：我们分析了表示的基因(transcriptomes)和翻译的蛋白质(专业版--teomes)在肌肉纸巾和激活的CD4+和五种类型的CD8+T淋巴细胞(T房间)，2糖尿病(T2DM)用Affymetrix微数组和集体spectrometry使遭到，并且把他们与匹配的非糖尿病的控制作比较。胰岛素受体(INSR)的基因表达，维生素D受体，胰岛素降级酶，Akt，胰岛素受体substrate-1(IRS-1)，IRS-2，葡萄糖transporter4(GLUT4)，并且glycolytic小径的酶被减少至少50%在T2DM比在控制。然而，有比在血浆房间glycoprotein-1的规定上面的双重的基因大，肿瘤坏死因素(在T2DM的TNF，和gluconeogenic酶比在控制。为INSR或TNF的基因silencing分别地导致了GLUT4的抑制或刺激。相应于上述翻译transcriptomes的分子的重量的Proteome侧面显示出在T2DM和控制之间的变化的不同模式。同时，在在肌肉和T2DM的激活的T房间之间的transcriptomes和proteomes的变化是可比较的。激活的T房间，类似于肌肉房间，表示胰岛素发信号和葡萄糖新陈代谢基因和基因产品。在结论，在T2DM的T房间和肌肉相对非糖尿病的控制在某些基因和基因产品的表示展出了差别。在transcriptomes的这些改变和在T2DM的proteomes可以涉及胰岛素抵抗。

简介：Interleukin-12(IL-12)isacriticalcytokinerepresentingthelinkbetweenthecellularandhumoralbranchesofhostimmunedefenseapparatus.IL-12-inducedcytotoxiclymphocyte(CTL)developmentisacentralmechanisminimmuneresponsesagainstintracellularinfectiousagentsaswellasmalignantgrowth.However,themolecularbasisoftumor-specificCTLresponsesmediatedbyIL-12remainspoorlydefined.Inthisstudy,weaddressedthisissueinacomprehensivemannertoprobeintoIL-12-inducedanti-tumorresponsesbyglobalgeneexpressionprofilingofmRNAexpressioninCD8+TcellsinatransplantablesyngeneicmousemammarycarcinomamodeltreatedornotwithrecombinantIL-12.AstrongtumorregressionwasinducedbytheIL-12treatment.AnintrospectionofdifferentialgeneexpressionatanearlystageoftheIL-12-initiatedCTLactivationrevealsinterestinggenesandmolecularpathwaysthatmayaccountforthemarkedtumorregression,andislikelytoprovidearichsourceofpotentialtargetsforfurtherresearchanddevelopmentofeffectivetherapeuticmodalities.Cellular&MolecularImmunology.2004;1(5):357-366.

简介：Inordertoelucidatethemolecularandimmunologicalmechanismsaswellasthepathogenesisofhemorrhagicfeverwithrenalsyndrome(HFRS),theCD8^+cytotoxicTlymphecytes(CTL)clonewasestablisheddirectlyfromperipheralbloodmononuclearcells(PBMC)ofpatientswithHFRS.TheactivitiesofCTLweredetectedasusualwithEBV-transformedlymphoblastoidcellline(BLCL)astargetcells.TheresultsshowedthattheCTLclonecouldrecognizedandkilledthetargetcellswithspecificityofnucleocapsidproteinofHantaanvirus(HTNVNP)withthecytotoxicitypercentagesof50.2%,25.4%and39.0%respectively.TheseresultsdemonstratedthattheantigenicepitopesofHTNVNPmainlylocatedontheC-temainaloftheviralnucleocapsidprotein.

简介：

简介：Toexploretheroleofnuclearfactor-κB(NF-κB)inthesignalpathwayofproteinkinaseC(PKC)regulatingtheproliferationandapoptosisofTlymphocytesinasthma.Tlymphocyteswereisolatedfromtheasthmaticmodelofguineapigsandtheasthmaticpatients.EithertheTcellsstimulatedwithPMAaloneorthosestimulatedwithPMAtogetherwithpyrrolidinedithiocarbamate(PDTC)wereincubatedfor1and24h.TheproliferationofandthepresenceofNF-κBinthecellsincubatedfor1hwereobservedbyMTTandimmunohistochemicalstaining,respectivelyAndthecellsincubatedfor24hwereobservedfortheapoptosisbyTUNEL.Alltheassayswereparalleledwithcontrols,andallthedatawereanalyzedstatisticallywiththesoftwareSAS.ThepercentageofcellsofnuclearpositivestainingofNF-scBandtheproliferationofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithPMAweresignificantlyhigherthanthoseofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithoutPMArespectively(P<0.01)andthoseofTlymphocytesfromnormalcontrolguineapigsandnormalcontrolpersonsstimulatedwithPMArespectively(P<0.01),andweresignificantlyreducedbyPDTC(P<0.01).TheapoptosisindexofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithPMAweresignificantlylowerthanthoseofTlymphocytesfromasthmaticguineapigsandasthmaticpatientsstimulatedwithoutPMArespectively(P<0.01)andthoseofTlymphocytesfromnormalcontrolguineapigsandnormalcontrolpersonsstimulatedwithPMArespectively(P<0.01),andweresignificantlyinducedbyPDTC(P<0.01).ThereweregoodpositivecorrelationbetweenthepercentageofcellsofnuclearstainingofNF-κBofTlymphocytesandtheproliferationofTlymphocytes(r=0.51-0.72,P<0.001),andalsogoodnegativecorrelationbetweenthepercentageofcellsofnuclearstainingofNF-scBandtheapoptosisindexofTlymphocytes(r=-0.55-0.71,P