负载肺癌A549抗原的树突状细胞对细胞因子诱导的杀伤细胞特异性激活研究
时间:2026-01-15
时间:2026-01-15
中国慢性病预防与控制2008年2月第16卷第1期ChinJPrevContrChronNon-communDis,February2008,Vol.16,No.1
23
【论著】
文章编号:1004-6194(2008)01-0023-04
负载肺癌A549抗原的树突状细胞对细胞因子诱导的
杀伤细胞特异性激活研究
苏征1,张灏1,李欣2,汤华2
摘要:目的
观察负载肺癌A549抗原的树突状细胞(DC)对细胞因子诱导的杀伤细胞(CIK)特异性肿瘤杀伤活性的作用。
方法由正常人富含淋巴细胞白膜分离、细胞因子诱导制备DC细胞和CIK细胞。用流式细胞术分析DC细胞和CIK细胞的表型。经混合淋巴反应和体外细胞毒性实验观察负载A549抗原的DC对CIK具有特异性激活作用。结果表型分析显示,
CIK细胞以CD3+CD56+自然杀伤细胞为主,成熟DC细胞高表达CD40、CD80、CD86和HLA-DR,并可刺激CIK细胞的增殖诱
导混合淋巴反应,而负载A549抗原的DC细胞能显著增强CIK细胞特异性杀伤靶细胞的能力(P<0.05)。小鼠注射CIK、 DC (70.17±CIK和AgDCCIK后的肿瘤直径分别为(65.34±12.33)、13.26)和(36.79±9.19)mm,后者的抗肿瘤作用较高(P<0.05)。结论抗原负载的DC细胞可活化CIK细胞,并使其具有特异性杀伤肿瘤细胞的能力。
关键词:树突状细胞;细胞因子诱导的杀伤细胞;激活中图分类号:R73
文献标识码:A
Cytokine-inducedKillerCellActivationbyDentriticCellsLoadedwiththeTumorAntigenfromHumanLungCancerCellLineA549Tianjin300070,China
Abstract:ObjectiveToexplorethespecificanti-tumoreffectofcytokine-inducedkillercell(CIK)activationbydentriticcells
SUZheng,ZHANGHao,LIXin,etal.TheBasicMedicineDepartment;TianjinMedicalUniversity,
(DC)loadedwiththetumorantigenfromhumanlungcancercelllineA549.MethodsCIKsandDCsderivedfromthehealthdonor'speripheralbloodmonocyte(PBMC)wereisolatedandinducedbythecytokineinvitro.DCsweregeneratedbycultureofad-herentcellsfromPBMCfor7daysinthepresenceofIL-4andGM-CSF.CIKsweregeneratedbycultureofnon-adherentcellsfor7or14daysinthepresenceofINF-γ,IL-2,IL-1α,andmouseanti-humanCD3monoclonalantibody.ThephenotypeofDCandCIKwasanalyzedbyFCM.TheactivityofDCwasevaluatedbyMLR;andthecytotoxicityofCIKwasassayedbyMTT.TheCIKexpres-sionprofileofcytokineandsignaltransductiongenesweredetectedbytheDNAmicro-arrayunderdifferentcircumstances.ResultsPhenotypicanalysisindicatedthatCD3+CD56+NKTcellswerepredominantintheCIKcellsgeneratedinthecurrentstudy,andthatDCcellsexpressedhighlevelsofCD40,CD80,CD86andHLA-DR.AsdemonstratedbyMTTassay,theCIKcellsproliferatedrapidly,andtheDCcellswereabletoinduceanMLR.Bothantigen-pulsedandunpulsedDCstimulatedtheproliferationofCIKcells,andnosignificantdifferencewasfoundbetweenthetwokindsofDCcells.U …… 此处隐藏:7941字,全部文档内容请下载后查看。喜欢就下载吧 ……