简介:Inthepaper,wegetthepreciseresultsofHájek-Rényitypeinequalitiesforthepartialsumsofnegativelyorthantdependentsequences,whichimprovetheresultsofTheorem3.1andCorollary3.2inKim(2006)andthestronglawoflargenumbersandstronggrowthratefornegativelyorthantdependentsequences.
简介:目的:构建天然免疫胞内识别受体核苷酸寡聚域1(NOD1)真核表达质粒。方法:NOD1基因片段经PCR扩增获得,经酶切后连接到真核表达载体pcDNA3/flag中,对挑选出的阳性克隆测序,将序列正确的重组质粒pnag—NOD1转染293T细胞,用Western印迹检测目的蛋白的表达,同时用NF-κB的萤光素酶报告基因检测NOD1蛋白的活性。结果:pflag-NOD1可以在真核细胞293T中表达,并可以增强NF-κB报告基因的转录活性。结论:构建了重组质粒pnag—NOD1,在细胞中表达NOD1后能够提高NF—κB转录的生物活性,为进一步研究NOD1的功能奠定了基础。
简介:Administrationofautoantigencanbeofvalueforpreventionofautoimmunediabetesandithasbeenspeculatedthatthecontrolpointofdendriticcells(DC)fortheinductionofperipheraltoler-ancemaybehighlyrelevant.WeexaminedthepropertiesofDCassociatedwithimmunesuppressioninNODmicebyinsulininjectionsubcutaneouslyandtheirabilitytosuppressdiabetestransferbydiabeto-geniceffectorcellsinsecondaryNOD-SCIDrecipients.OurdatashowedthatthesurfaceexpressionsofMHCⅡandCD86onNOD-derivedDCwereincreasedafterinsulintreatmentcomparedwiththoseonPBScontrolledmice.ThedendriticcellswithamaturephenotypeandincreasedMLRstimulationadop-tivelytransferredimmunetolerogeniceffectsonsecondaryNOD-SCIDmice,whichwereassociatedwithsignificantlygreaterIL-10,TGF-betaproductionandCD4~+CD25~+TdifferentiationfromsplenocytescomparedwithNOD-SCIDcontrolrecipients.Moreover,treatmentwithDCremarkablydecreasedtheincidenceofdiabetesinsecondaryrecipients.TheseresultssuggestthatasubtypeofDCgeneratedbyinsulinsubcutaneoustreatedNODmiceconferspotentialprotectionagainstdiabetesthroughpolarizingtheimmuneresponsetowardsaTh2regulatorypathway.
简介:摘要目的探讨来氟米特对干燥综合征模型NOD鼠唾液腺分泌功能减退的治疗作用。方法将NOD鼠随机分配为4组:预防用药组、预防对照组、治疗用药组、治疗对照组;检测毛果芸香碱刺激后唾液流率变化;苏木精和伊红染色后比较平均浸润灶数目及面积的变化;流式细胞术检测颌下腺、脾脏组织中CD3+T、CD4+T、CD8+T、CD44+CD62L-CD4+T、CD19+B、CD138+B细胞水平的变化;CBA法检测血清炎症因子TNF-α、IL-17A、IL-6水平变化。结果预防用药及治疗用药组唾液流率(t=-5.81,P<0.001;t=-3.61,P<0.05)、浸润灶平均数目(t=3.95,P<0.01;t=4.94,P<0.001)、浸润灶平均面积(t=3.18,P<0.05;t=2.35,P<0.05)均具有明显改善。颌下腺组织中CD3+CD4+T(t=2.39,P<0.05;t=3.82,P<0.01)、CD44+CD62L-CD4+T(t=3.53,P<0.05;t=3.36,P<0.05)细胞明显下调。脾组织中CD3+T(t=6.08,P<0.001;t=2.76,P<0.05)、CD3+CD4+T(t=3.73,P<0.05;t=2.39,P<0.05)、CD19+B(t=5.88,P<0.001;t=4.23,P<0.01) 、CD138+B(t=4.30,P<0.001;t=4.46,P<0.01)细胞也均明显下降。此外,用药组小鼠血清IL-17A水平均降低(t=4.15,P<0.01;t=3.36,P<0.01),预防用药组TNF-α水平下降(t=4.56,P<0.001),但IL-6水平变化无统计学意义。结论本研究提示来氟米特可预防、改善NOD鼠唾液腺功能减退及抑制体内免疫活化,为评估来氟米特对干燥综合征的治疗作用提供了理论依据。