简介：CD40和它的血缘的ligand(CD40L)是支持inflammatory和有免疫力的回答的一双管理者。在中央神经系统(CNS)，CD40在许多房间上被表示，包括脉管的endothelial房间，光滑的肌肉房间，星形细胞和microglia(大脑巨噬细胞，是最敏感的房间打字对CD40ligand作出回应)。在渗入T淋巴细胞和另外的居民CNS房间介绍的microglia和CD40L上的CD40之间的相互作用触发支持cytokines，chemokines和神经毒素的一个宽数组的生产的一系列细胞内部的发信号事件。因此，两个分子在CNS用作支持inflammatory和有免疫力的回答的放大器并且为疾病的治疗学的干预组成重要分子的目标。

简介：在维持平衡外部有免疫力的system.Recent的一个重要角色学习的CD4+CD25+规章的T(TR)房间玩证明了TR房间可以也在压制反肿瘤免疫者反应起一个关键作用。以便调查TR极化上的肿瘤免疫者微型环境和它的影响，糟糕产生免疫性的肿瘤房间线D5(C57BL/6，H-2b)，产生免疫性的肿瘤房间线FBL3(C57BL/6，H-2b)并且H22BALB/c，H-2d)被用来建立syngeneic/allogeneic，糟糕产生免疫性/产生免疫性的混合淋巴细胞肿瘤房间文化(MLTC)。我们的结果表明在告知的splenocytes与D5肿瘤房间刺激了的syngeneic的MLTC的CD4+CD25+T房间的比例与H22房间比那高(0.43%对0.044%，并且类似的结果在与.Thesplenocytes从更高表明的房间比从D5肿瘤的allogeneicMLTC，房间，和splenocytes刺激了机智的CD4+CD25+房间分配的D5肿瘤的syngeneicMLTC与上层清液刺激了的D5肿瘤房间(0.39%对0.04%)刺激的allogeneicsplenocytes出现了TGF-1和Th2面向的cytokines(IL-4和IL-10)在糟糕产生免疫性的肿瘤房间的syngeneicMLTC的上层清液被统治。我们的结果为学习位于肿瘤免疫者监视下面的机制以及为肿瘤免疫疗法提供了有用信息。

简介：CD3-specificmonoclonalantibodywasthefirstoneusedforclinicalpracticeinfieldoftransplantation.Recently,renewedinterestshaveelicitedinitscapacitytopreventautoimmunediabetesbyinducingimmunetolerance.Inthisstudy,wetestedwhetherthisantibodycanalsobeusedtotreatanotherkindofautoimmunediseasemyastheniagravis(MG)andexploredthepossiblemechanisms.MGiscausedbyanautoimmunedamagemediatedbyantibody-andcomplement-mediateddestructionofAChRattheneuromuscularjunction.WefoundthatadministrationofCD3-specificantibody(Fab)2toananimalmodelwithexperimentalautoimmunemyastheniagravis(EAMG)(B6micereceived3timesofAChR/CFAimmunization)couldnotsignificantlyimprovetheclinicalsignsandclinicalscore.Whenthepossiblemechanismsweretested,wefoundthatCD3antibodytreatmentslightlydown-regulatedtheT-cellresponsetoAChR,modestlyup-regulationthemusclestrength.AndnosignificantdifferenceinthetitersofIgG2bwasfoundbetweenCD3antibodytreatedandcontrolgroups.ThesedataindicatedthatCD3-specificantibodywasnotsuitablefortreatingMG,anantibody-andcomplementmediatedautoimmunedisease,afterthisdiseasehasbeenestablished.TheroleofCD3-specificantibodyintreatingthiskindofdiseaseremainstobedetermined.

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：CD134,amemberofthetumornecrosisfactorreceptorsuperfamily,playsacrucialroleinTcellsurvival.Inthisstudy,peripheralbloodmononuclearcells(PBMCs)stimulatedwithphytohemagglutinin(PHA,50μg/ml)weretreatedbyCD134mAb(1μg/ml,5μg/ml,10μg/ml)for6h,12h,24hand48h.ThelevelofperforinmRNAwasmeasuredbyreversetranscription-polymerasechainreaction(RT-PCR)technique.OurdatashowedthattheexpressionofperforinmRNAinPBMCswasdown-regulatedbyCD134mAbinadose-dependentmannerinrangeof1μg/mlto5μg/mlanddroppeddowntoitsminimumon24h(p＜0.05).ThelevelofperforinmRNAreachedaplateauwhentheconcentrationofCD134mAbexceeded5μg/ml.Inconclusion,CD134mAbcaninhibitperforinexpression,whichmayenhancetheabilityofTcellsforsurvival.

简介：CD137,acostimulatoryfactorofTNFRfamily,isexpressedonactivatedTcellsandfreshlyisolatedmousedendriticcells(DCs).Todate,thereareonlylimiteddatadealingwiththeexpressionandtheeffectofCD137onhumanDCs.WereportinthisworkthatCD137cancoexpresswithCD137Lonimmatureperipheralblood-derivedhumanDCs(9.77%).ThematureDCsstimulatedbyLPSshowedamuchhigherlevelofCD137expression(36.06%).LigationofCD137onthesurfaceofDCswithanti-CD137monoclonalantibody(mAb)couldenhancethedirectanti-tumoreffectmediatedbyhumanDCsinvitro.Theagonisticanti-CD137mAbwasabletoelevatebyabout20%oftheDC-mediatedinhibitionoftumorgrowthinfivetumorcelllines.Theseresultsindicatethattheapplianceofanti-CD137mAbmightbeusedasanewstrategyfortumorimmunotherapy.Cellular&MolecularImmunology.2004;1(1):71-76.