简介：TodeterminetheregulatoryeffectsofestrogenandcytokineIL-6andIL-8onthegrowthofepithelialovariancancer(OVCA),wefirstexaminedthestatusofestrogenreceptors(ERαandERβ),IL-6receptor(IL-6Rαandgp130),andIL-8receptor(IL-8RAandIL-8RB)onfiveepithelialOVCAcelllinesbysemiquantitativeRT-PCRandWesternblotanalysis.Resultsshowedthattheexpressionsofthesereceptorswerevariableonthefivecells.ThoseOVCAcellsexpressingthereceptorswereselectedtostudyrelatedmolecularmechanism.MTTassaywasperformedtoobservetheeffectsof17β-estradiol(E2),IL-6andIL-8oncellproliferation.WediscoveredthatE2markedlypromotedtheproliferationofCAOV-3andOVCAR-3cellinatime-anddose-dependentmanner.Tamoxifen(Txf),anERinhibitor,completelyblockedtheproliferationoftheE2-inducedcells,andIL-6-or/andIL-8-neutralizingantibodyonlyshowedpartiallyblockingactivity.IL-6andIL-8wereabletosignificantlystimulateCAOV-3andOVCAR-3cellproliferationinatime-anddose-dependentmanner,whichhadapotentialsynergisticeffectonCAOV-3cellsbutnotonOVCAR-3cells.Thecellproliferationinducedbythesetwocytokineswasabolishedcompletelybytheirspecificneutralizingantibodies,partiallybyTxf,butnotbyunrelatedgoatIgG.Takentogether,ourresultssuggestedthatestrogen,IL-6andIL-8couldmodulateOVCAgrowthbyformingareciprocalcascadewithamplifyingeffect.Cellular&MolecularImmunology.

简介：包括长期的感染，自体免疫的疾病和癌症，很长期的人的疾病的致病经常包含坚持的、未解决的煽动性的回答。决定尖锐煽动性的回答的变换进一个长期的过程的分子的机制难倒研究人员许多年了。最近的研究揭示那B7-H1(CD274，PD-L1)，一个最新识别的co-stimulatory分子，拥有天真的T房间的合作刺激和激活的受动器T房间的抑制的双功能。异常细胞的表示和B7-H1的deregulated功能在长期的病毒、细胞内部的细菌的感染期间被报导了，以及在许多自体免疫的疾病和癌症。重要地，B7-H1的双功能的解除管制看起来与被联系一延长，由为激活诱惑天真的T房间并且阻抑的不完全的有免疫力的反应激活受动器T房间。而且，指向B7-H1信号的策略的开发提供一条新、有希望的途径操作与长期的发炎联系的破坏疾病。因此，B7-H1可以在煽动性的回答的慢性起一个批评immunoregulatory作用。

简介：BandTlymphocyteattenuator(BTLA),identifiedasanimmuneinhibitoryreceptorrecently,playswidespreadrolesonTandBcells.EmergingevidencehasgeneratedplentifulinformationonthemechanismswhichBTLAmediatesnegativeregulationinimmuneresponsesandinvolvesinavarietyofphysiologicalandpathologicalprocesses.TheexplorationofthebiologicalmechanismsandregulationofBTLAwillopenpossibilitiesonnoveltherapeuticstrategiesinimmune-relateddiseases.

简介：NF-κBisatranscriptionfactorofeukaryote,fivemembersofwhosefamilyinmammalsandthreeindrosophila.TranscriptionfactorsoftheNF-κfamilyareactivatedinresponsetosignalsthatleadtocellgrowth,differentiation,apoptosisandotherevents.NF-κBtakespartinexpressionofnumerouscytokinesandadhesionmoleculeswhicharecriticalelementsinvolvedintheregulationofimmuneresponses.Inthisreview,wefocusonourcurrentunderstandingofNF-κBsignalpathwayanditsroleintheinnateandadaptiveimmuneresponsesinwhichthesetranscriptionfactorshaveakeyregulatoryfunction.Furthermorewereviewwhatiscurrentlyknownabouttheireffectsassociatedwithapoptosis.Cellular&MolecularImmunology.2004;1(5):343-350.

简介：ThemolecularmechanismsforNF-κBsignalingtransductionandtranscriptionhavebeenthemostattractivesubjectsforbothbasicresearchandpharmaceuticalindustriesduetoitsimportantrolesinbothphysiologicalandpathogenesis,particularlythecloseassociationofdysregulatedNF-κBwithtumorgenesisandinflammation.SeveralnovelintracellularmoleculareventsthatregulateNF-κBactivityhavebeendescribedrecently,includingthediscoveryofanalternativesignalingpathwaythatappearsinducingaspecificsubsetgenesinvolvedinadoptiveimmuneresponse.Multi-levelandmulti-dimensionalregulationofNF-κBactivitybyphosphorylationandacetylationmodificationshaveunveiledandbecamethehottesttargetsforpotentiallytissuespecificmolecularinterventions.AnotheremergingmechanismforNF-κB-responsivegene'sregulationwhereNF-κBparticipatesthetranscriptionalregulationindependentofitscognateregulatorybindingsitewithinthetargetgene'spromoterbutfacilitatingthetransactionactivityofotherinvolvedtranscriptionfactors,thatimplicatedannoveltranscriptionalactivitiesforNF-κB.Thus,thecurrentreviewwillfocusontheserecentprogressesthathavebeenmadeonNF-κBsignalingtransductionandtranscription.Cellular&MolecularImmunology.2004;1(6):425-435.

简介：肝炎B病毒(HBV)感染与传染virions和非传染的空表面抗原粒子的版本首先在hepatocytes发生在肝进血液。HBV复制是non-cytopathic。短暂感染运用几个月，和长期的感染的一堂功课经常是终生的。长期的感染能与肝硬化和hepatocellular癌导致肝失败。抵销anti-HBs抗体由在感染的主人包含感染的传播并且便于病毒的粒子的移动和破坏从HBV感染在恢复起一个关键作用，这通常被接受。然而，对病毒的抗原的T房间反应开始的有免疫力的反应在HBVinfection.The为病毒的清理和疾病致病也是重要的病毒的蛋白质，HBsAg，微粒HBcAg，和nonparticulateHBeAg的三种结构的形式，可以优先地得到不同Th房间子集。在不同HBV感染地位的anti-HBs，anti-HBc，和anti-HBe的不同IgG亚纲侧面被揭示。而且，在长期的搬运人的不同IgG亚纲侧面没随着不同中高音和著名计算机生产厂商层次变化并且可以反映刺激抗原之间的差别，有免疫力的反应，并且病毒的疾病的阶段并且在人的HBV感染的高风险为个人为疫苗和预防处理的使用提供基础。这评论阐明在短暂、坚持的感染期间导致的有免疫力的回答的详细理解，和在有HBV感染的病人的免疫疗法和immunodiagnosis的发展，和减少肝的可能的工具损坏。

简介：Oligodeoxynucleotides(ODN)containingunmethylatedCpGdinucleotidesincontextsofuniquesequence(CpGmotifs)isactiveasadjuvantininductionofcellularandhumoralimmuneresponsesinyoungmice.Todate,thereareonlylimitedreportsabouteffectofCpGODNonimmuneresponsesagainsthepatitisB(HB)infectioninagedmice.Ourstudiesdemonstratedthereweresignificantincreasesinsecretingoftotalanti-HBIgG,IgG1andIgG2a,aswellasofIL-12andIFN-γ,whenCpGODNswereinjectedtogetherwithhepatitisBantigeninagedmice.Moreover,CpGODNcouldstimulateproliferationofspleenlymphocytesinadose-dependentmanner.Takentogether,theresultsweobtainedindicatethattheaddingofCpGODNintothevaccineantigenmightbeusefulindevelopmentofmoreeffectivevaccinationforinducinganti-HBvirusresponsesintheelderly.

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：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：Theworkistoexploretherelationshipbetweenthelevelsofcytokines(IL-1βandIL-6)inC57BL/6JmicetreatedwithMPTPandbrainlateralization.Byusingpawpreferencetest,right-pawed,left-pawedmicemodelswereestablished.Followingsingleinjectionof1-methyl-4-pheny1-2,3,6-tetrahydropyrid(MPTP)(40mg/kg)toimpairdopaminergicneuron,enzymelinkedimmunosorbentassay(ELISA)kitswereusedfordetectionofplasmalevelsofcytokines.TheresultsshowedthatinsalinetreatedC57BL/6Jmice(control),therewasnoobviousdifferenceobservedbetweenleft-pawedandright-pawedmiceinplasmalevelsofIL-1βandIL-6.InMPTPtreatedmice,therewasnodifferencebetweenlevelofIL-1βinleft-pawedmiceandthatinright-pawedonesinstatistics,thatis,theywereincreasedonday1andday3,butdecreasedonday6.TheplasmalevelofIL-6waslowerinleft-pawedthanthatinright-pawedmice(p＜0.005)afterMPTPtreatment.Onday1andday3,thelevelofIL-6wasalmostthesameascontrol;onday6,itwassignificantlyincreased,higherthanthatofcontrol(p＜0.001)inleft-pawedmice.Whileinright-pawedmice,onday1andday3,itwasnodifferentfromcontrol,too.Andonday6,itsignificantlyincreasedincomparedwithcontrol(p＜0.005).Inconclusion,thelevelofplasmaIL-6ofC57BL/6JmicetreatedwithMPTPincreased.ThevariationofIL-6wascorrelatedtobrainlateralization.

简介：Quercetinisaherbalflavonoidderivedfromvariousfoodsofplantoriginandplaysaroleinanti-inflammation.Althoughanumberofresearchesinthefieldhavebeendone,themechanismofanti-inflammatoryeffectofquercetinshouldbefurtherclarified.Inthepresentstudy,weinvestigatedtheeffectsofquercetinonIL-6productionbyLPS-stimulatedneutrophilsinhuman.Neutrophilswerewerepre-treatedwithquercetinatthefinalconcentrationsofrangingfrom0-80μMfor30min,ornottreated,andthenincubatedinthepresenceorabsenceoflipopolysaccharide(LPS)atafinalconcentrationof100ng/mlforindicatedtime.ThesecretionlevelofIL-6intheculturesupernatantswasassayedbyELISA,theintracellularlevelofIL-6wasdetectedbyflowcytometryandtheexpressionofIL-6mRNAwasanalyzedbyRT-PCR.TheexperimentresultsshowedthatneutrophilsculturedwithmediumorquercetinalonedidnotexpressIL-6,butLPS(100ng/ml)inducedIL-6expressionofneutrophils.However,afterpre-treatmentofneutrophilswithquercetin(40μM)for30min,theinducibleeffectsofLPSontheincreaseofIL-6secretion,intracellularIL-6levelandIL-6mRNAexpressionbyneutrophilswereabrogated.IL-6isoneoftheimportantpro-inflammatoryfactors,especiallyinearlyphageofinflammation.Thus,ourdatasuggestedthatquercetinmightexertitsanti-inflammatoryeffectthroughnegativelymodulatingpro-inflammatoryfactors,suchasIL-6.TheinhibitoryeffectsofquercetinonIL-6productionbyneutrophilsmayprovideatheoreticalbasisonfuturetherapyofinflammation.

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：Interleukin-6(IL-6)-deficientmicearepronetoethanol-inducedapoptosisandsteatosisintheliver;however,theunderlyingmechanismisnotfullyunderstood.Mitochondrialdysfunctioncausedbyoxidativestressisanearlyeventthatplaysanimportantroleinthepathogenesisofalcoholicliverdisease.Therefore,wehypothesizethattheprotectiveroleofIL-6inethanol-inducedliverinjuryismediatedviasuppressionofethanol-inducedoxidativestressandmitochondrialdysfunction.Totestthishypothesis,weexaminedtheeffectsofIL-6onethanol-inducedoxidativestress,mitochondrialinjury,andenergydepletionintheliversofIL-6(-/-)miceandhepatocytesfromethanol-fedrats.Ethanolconsumptionleadstostrongerinductionofmalondialdehyde(MDA)inIL-6(-/-)micecomparedtowild-typecontrolmice,whichcanbecorrectedbyadministrationofIL-6.Invitro,IL-6treatmentpreventsethanol-mediatedinductionofreactiveoxygenspecies(ROS),MDA,mitochondrialpermeabilitytransition(MPT),andethanol-mediateddepletionofadenosinetriphosphate(ATP)inhepatocytesfromethanol-fedrats.AdministrationofIL-6invivoalsoreversesethanol-inducedMDAandATPdepletioninhepatocytes.Finally,IL-6treatmentinducesmetallothioneinproteinexpression,butnotsuperoxidedismutaseandglutathioneperoxidaseinculturedhepatocytes.Inconclusion,IL-6protectsagainstethanol-inducedoxidativestressandmitochondrialdysfunctioninhepatocytesviainductionofmetallothioneinproteinexpression,whichmayaccountfortheprotectiveroleofIL-6inalcoholicliverdisease.

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简介：Suppressorofcytokinesignaling3(SOCS3)wasreportedasafeedbackinhibitorofcytokinereceptorsignalingbyinhibitingtheJAK-STATsignaltransductionpathway.Wesoughttotesttheanti-endotoxicsepticshockeffectofliposomemediatedgenedeliveryofSOCS3inalethalendotoxicshockmousemodel.BALB/cmicewereinjectedintraperitoneallywith200μgpcDNA3.1-SOCS3cationicliposomes,whilepcDNA3.1-IL-10andemptyvectoraspositiveandnegativecontrolrespectively.Forty-eighthoursaftergenedelivery,micewerechallengedwith4μgofE.coli0127:B8LPSand18mgD-GalNadministeredi.p.90minlater,serumTNF-αlevelwasdetermined.Survivaloverthenext48hwasevaluated.Peritonealmacrophagesfromsurvivalmicewerestimulatedinvitrowith1μg/mlLPSfor18h,andthesupernatantswereharvestedfordeterminationoftheamountofTNF-α.WefoundthatgenedeliveryofSOCS3significantlyincreasethemousesurvivalratefrom27.8±9.6%ofcontrolgroupto61.1±9.6%(p＜0.01).Incomparisonwithcontrolgroup(218±13pg/ml)andshamdeliverygroup(219±22pg/ml),genedeliveryofSOCS3reducedthelevelofserumTNF-α(68±9pg/ml)significantly(p＜0.01).Furthermore,genedeliveryofSOCS3displayedthecapacityofpreventionoftoleranceofperitonealmacrophagestoLPS.ThesefindingssuggestthatgenedeliveryofSOCS3mediatedbyliposomeisapromisingapproachforendotoxicsepticshocktreatment.Cellular&MolecularImmunology.

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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：IthasbeenrevealedthatpolyⅠ:CisapotentstimulatorforNKcells,whichcaninduceNKcellrapidactivationandpreferentialaccumulationintoliver.However,theprocessmediatingtheinfluxofNKcellsremainsobscure.Inthisstudy,wefoundthatpolyⅠ:CadministrationincreasedtheportionandabsolutenumberofNKcellsinliver,butlargelydecreasedthoseinspleen.Therewerenoobviouschangesoftheselymphocytesinotherimmuneorgans.TheresultsfromsplenicadoptivetransferandsplenectomyshowedthattherecruitedspleenNKcellscontributedtotheaccumulationofNKcellsinliver,andthisprocesswasregulatedbytheproductionofchemokinesandthepresenceofTcells.Thisinvestigationwillhelptounderstandtheenhancedimmunecellrecruitmentinliveruponviralinfection.

简介：生来的杀手(NK)房间是骨头导出髓的淋巴细胞。他们生产cytokines调整获得的免疫的发展。鉴于他们在母亲胎儿的接口的累积，子宫的生来的杀手(uNK)房间也被认为在怀孕期间起必要作用。我们的结果在子宫的子宫内膜，肝，怒气和外部血由NK房间比较了cytokine分泌物侧面的差别，并且由uNK房间集中了于cytokines分泌物。在怀孕鼠标的子宫的子宫内膜的IFN-和TNF-的表达式是比在肝的那些低的，这被表明，但是他们在怀孕期间显著地增加。我们的学习证明uNK房间的数字在怀孕期间显著地被增加。他们比另外的导出器官的NK房间，和他们也分泌IL-4和IL-5的次要的数量的生产了更多的IFN-和TNF-。结果显示uNK房间生产的IFN-和TNF-保证了成功的怀孕进步。