简介：Thegeneralprinciplefortumorcellstoescapefromimmunesurveillanceistopreventtumorantigensfrombeingrecognizedbytheimmunesystem.Manymethodshavebeendevelopedtoincreasetheimmunogenecityofthetumorcells.Themostefficientmethodsareabletoforcetumorcellstopresenttheirowntumorantigenstotheimmunesystem.StimulatingThcellsbyconvertingtumorcellsintoMHCclassⅡ+/Ii-antigenpresentingcellsisoneofthemostefficienttechnologies.Usingantisensemethods,wesuppresstheexpressionoftheIiproteinthatnormallyco-expresseswithMHCclassⅡmoleculesandblockstheantigenicpeptidebindingsiteofMHCclassⅡmoleculesduringsynthesisintheendoplasmicreticulum.Insuchtumorcells,the'unprotected'MHCclassⅡmoleculespickupendogenoustumorantigenicpeptides,whichhavebeentransportedintotheERforbindingtoMHCclassⅠmolecules.SimultaneouspresentationoftumorantigensbybothMHCclassⅠandⅡmoleculesgeneratesarobustandlong-lastinganti-tumorimmuneresponse.MHCclassⅡ+/Ii-tumorcellsarepotenttumorcellvaccinesandalsocureasignificantnumberofanimalswithrenalandprostatetumors.Wehavedevelopedanalogoushumangenevectorsthataresuitableformostpatientsandcancers.

简介：Dendriticcells(DCs)arerecognizedasthemostpotentantigen-presentingcells(APCs)withtheabilitytostimulatena(i)verestingTcellsandinitiateprimaryimmuneresponses.DCsarepoisedtocaptureantigen(Ag),migratetodraininglymphoidorgans,and,afteraprocessofmaturation,selectAg-specificlymphocytestowhichtheypresenttheprocessedAg,therebyinducingimmuneresponses.NumerousstudiesindicatedthatimmunotherapiesutilizingDC-presentingtumor-associatedantigenscansafelybeadministeredtocancerpatientsandinducesignificantimmunologicandclinicalresponses.Moreover,ithasbeendemonstratedthatDCsarerelatedtoclinicalstage,invasion,metastasisandprognosisofgastriccancer.DC-basedtumorvaccinesbecomeaneweffectiveimmunoadjuvanttherapyforgastriccancer.Cellular&MolecularImmunology.2004;1(5):351-356.

简介：interleukin-24(IL-24)能在人的癌症的一个大系列导致apoptosis，是记录得好的MDA-7/IL-24基因的导出的房间线，而是效果在未知的老鼠黑瘤房间遗体上转。IL-24(pEGFP-IL-24)的真核细胞的表示plasmid被DNA再结合技术构造。再结合plasmid和空向量是进B16F0房间的transfected，IL-24的表情被LSM决定，B16F0房间的增长被MTT试金，和apoptosis率测量，B16F0房间的房间周期分发被FCM测量。在老鼠固体肿瘤的IL-24基因transfection的禁止的效果被观察并且测量。与控制相比，B16F0房间的增长被transfection与pEGFP-IL-24禁止，transfected房间的G2/M阶段也是increased.Moreover，在与pEGFP-IL-24与B16F0房间transfected接种以后，有可检测的肿瘤的鼠标的百分比被减少。在老鼠模型的肿瘤的生长率显著地与控制相比在IL-24基因治疗组被禁止。B16F0细胞的增长被pEGFP-IL-24的pEGFP-IL-24transfection.Theintratumor注射禁止能显著地在老鼠禁止稳固的肿瘤的生长。

简介：为了分析有免疫力的反应到老鼠的鼠科的hepatocarcinomaHca-F，与热吃惊使免疫(HSP70)蛋白质70源于elemene组合肿瘤Hca-F的房间疫苗(EC-TCV)，HSP70被自动数据处理从EC-TCV孤立亲密关系层析。老鼠intraperitoneally与HSP70被使免疫三次，怒气房间被取样。为房间，他们对Hca-F的增长和cytotoxicity与MTT试金被测量，他们的显型与流动cytometry被分析。有HSP70的使免疫的鼠标的怒气房间比与EC-TCV使免疫的鼠标的比正常控制鼠标，而是更少的有势力的对Hca-F和增长展出了更多的有势力cytotoxicity。在三个组之中，在与HSP70(35.5%)使免疫的老鼠的T淋巴细胞的百分比在正常老鼠与6.25%相比是最高的，并且28.4%与EC-TCV在老鼠使免疫。从EC-TCV导出的HSP70的免疫能得到有势力免疫者反应到Hca-F。HSP70是对Hca-F导致反肿瘤免疫者回答的元素之一。细胞与分子的免疫学。2006；3(4):291-295。

简介：Directintratumoralintroductionoftherapeuticorregulatorygenesisadevelopingtechnologywithpotentialapplicationforcancergenetherapy.Macrophageinflammatoryprotein-1beta(MIP-1β)isachemokinewhichcanchemoattractimmunecellssuchasTcells.Inthepresentstudy,murinecolorectaladenocarcinomaCT26cellsweretransfectedwitharecombinantadenovirus(AdhMIP-1β)carryingthehumanMIP-1βgene.24hpost-transfection,hMIP-1βlevelsreachedapproximately980pg/mlinsupernatantsof106hMIP-1β-transfectedCT26cells.Moreover,thesupernatantsexhibitedchemotacticactivityforCD8+Tcells,CD4+Tcells,NKcellsandimmatureDCs.IntratumoralinjectionofAdhMIP-1βsignificantlyinhibitedtumorgrowthandprolongedthesurvivaltimeoftumor-bearingmice.IntratumoralhMIP-1βgenetransferalsoinducedpowerfultumor-specificCTLresponsesinvivo.ThetherapeuticeffectsofhMIP-1βgenetherapyweregreatlyreducedfollowinginvivodepletionofbothCD4+andCD8+Tcells,butwereunaffectedbydepletionofsingleTcellsubsets.ImmunecelldepletionexperimentsalsorevealedthatNKcellsplayedanimportantroleinhMIP-1β-inducedantitumorresponses.TheseresultssuggestthatintratumoralexpressionofhMIP-1βhasthepotentialeffecttoinducehostantitumorimmunityandmayprovetobeausefulformofcancergenetherapy.

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：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.