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：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。

简介：Transplantrejection,liketolerance,isaTcell-dependentevent.ThereiscompellingevidencetosuggestthatinductionoftransplanttoleranceisanactivelylearnedprocessinwhichTcellsneedtoengagewiththealloantigensinordertolearntotoleratetheallograft.AfamilyofcytokineswhosereceptorsusethesameIL-2receptorγcchain(alsocalledthecommonγc)playsanimportantroleinregulatingmultipleaspectsoftheallograftresponse(I.e.Rejectionvs.Tolerance).ItisundeniablethatγccytokinescandriveclonalexpansionandeffectormaturationofalloreactiveTcells,andtherefore,targetingsuchcytokinesortheirreceptorcomponentsremainsanattractivewayofblockingtransplantrejection.However,wejuststartedtoappreciatethatγccytokinesalsoregulatetheacquisitionoftransplanttoleranceviaprogrammingactivatedTcellsforapoptoticcelldeathandviaguidingtheevolutionofregulatoryTcells.Thus,understandingpreciselytheroleofγccytokinesinregulatingTcellhomeostasisandTcellregulationiscriticallyimportantintheinductionoftransplanttolerance.

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：Thec-JunN-terminalkinases(JNKs)areclassicstress-activatedproteinkinases.ManycellularstresseshavebeenshowntostimulateJNKactivation.Inthisreview,wefocusonribotoxicstressesbasedontheirmultiplebiologicalpotenciesincludinganti-HIV-1activity.Someofthefunctionsofribotoxinsandthesignalingtransductionpathwaythatmediatedarementioned.Differentfromotherstimulators,ribotoxicstressesactonspecialmotifsof28SrRNAintranslationallyactivemammalribosomes.BindinganddamagingonthemotifleadstoJNKactivationandsubsequentlybiologicalresponsetothesignalinitiator,whichisnamedribotoxicstressresponse.

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.

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：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.