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简介：树枝状的房间(DC)在造血的房间的一张次要的人口，生产类型我干扰素(IFN)和另外的cytokines并且为天生的免疫是必要的。他们也是有势力抗原演讲者并且调整适应免疫。在DC子类型血浆之中似细胞的DC(pDC)生产类型的最高的数量我IFN。另外，象IL-12和IL-10那样的支持inflammatory和反煽动性的cytokines响应象发信号的受体(TLR)一样并且在病毒的感染之上的代价在DC被导致。在IRF家庭的蛋白质控制DC活动的许多方面。IRF-8和IRF-4为DC开发是必要的。他们差别控制四个DC子集的开发。IRF-8-/-老鼠大部分缺乏pDC和CD8alpha+DC，当IRF-4-/-老鼠缺乏CD4+DC时。IRF-8-/-，IRF4-/-，两倍猛烈老鼠有仅仅很少CD8a-CD4-DC那缺乏MHCII。IRF蛋白质也控制类型我在DC的IFN正式就职。IRF-7，在TLR发信号之上激活不仅在pDC，而且在常规DC(cDC)为IFN正式就职被要求，non-DC房间打字。IRF-3贡献在成纤维细胞感应的IFN，在在DC感应的IFN是非必需的。我们的最近的证据揭示那种类型我在DC感应的IFN非常依赖于IRF-8，它在DC在IFN基因正式就职的反馈阶段行动。类型我在pDC感应的IFN被MyD88调停依赖发信号小径，并且不同于在另外的房间采用的小径，它主要依靠TLR3和RIG-I家庭蛋白质。另外的支持inflammatorycytokines以一种IRF-5依赖方式被生产。然而，IRF-5没为IFN正式就职被要求，建议为类型的正式就职的分开的机制的存在我IFN和其它支持inflammatorycytokines。激活的DC接着生产的IFN和另外的cytokines预付DC成熟并且改变DC的显型和功能。这些过程也是可能的被IRF家庭蛋白质管理。

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简介：Uponencounteringtheantigen(Ag),theimmunesystemcaneitherdevelopaspecificimmuneresponseofenteraspecificstateofunresponsiveness,tolerance.TheresponseofBcellstotheirspecificAgcanbeactivationandproliferation,leadingtotheimmuneresponse,oranergyandactivation-inducedcelldeath(AICD),leadingtotolerance.AICDinBlymphocytesisahighlyregulatedeventinitiatedbycrosslinkingoftheBcellreceptor(BCR).BCRengagementinitiatesseveralsignalingeventssuchasactivationofPLCγ,Ras,andPI3K,whichgenerallyspeaking,leadtosurvival.However,intheabsenceofsurvivalsignals(CD40orIL-4Rengagement),BCRcrosslinkingcanalsopromoteapoptoticsignaltransductionpathwayssuchasactivationofeffectorcaspases,expressionofpro-apoptoticgenes,andinhibitionofpro-survivalgenes.ThecomplexinterplaybetweensurvivalanddeathsignalsdeterminestheBcellfateand,consequently,theimmuneresponse.

简介：ApoptosisproducedinBcellsthroughFas(APO-1,CD95)triggeringisregulatedbysignalsderivedfromothersurfacereceptors:CD40engagementproducesupregulationofFasexpressionandmarkedsusceptibilitytoFas-inducedcelldeath,whereasantigenreceptorengagement,orIL-4Rengagement,inhibitsFaskillingandinsodoinginducesastateofFas-resistance,eveninotherwisesensitive,CD40-stimulatedtargets.SurfaceimmunoglobulinandIL-4RutilizeatleastpartiallydistinctpathwaystoproduceFas-resistancethatdifferentiallydependonPKCandSTAT6,respectively.Further,surfaceimmunoglobulinsignalingforinducibleFas-resistancebypassesBtk,requiresNF-κB,andentailsnewmacromolecularsynthesis.TerminaleffectorsofBcellFas-resistanceincludetheknownanti-apoptoticgeneproducts,Bcl-XLandFLIP,andanovelanti-apoptoticgenethatencodesFAIM(FasApoptosisInhibitoryMolecule).faimwasidentifiedbydifferentialdisplayandexistsintwoalternativelysplicedforms;faim-Sisbroadlyexpressed,butfaim-Lexpressionistissue-specific.TheFAIMsequenceishighlyevolutionarilyconserved,suggestinganimportantroleforthismoleculethroughoutphylogeny.InducibleresistancetoFaskillingishypothesizedtoprotectforeignantigen-specificBcellsduringpotentiallyhazardousinteractionswithFasL-bearingTcells,whereasautoreactiveBcellsfailtobecomeFas-resistantandaredeletedviaFas-dependentcytotoxicity.InadvertentoraberrantacquisitionofFas-resistancemaypermitautoreactiveBcellstoescapeFasdeletion,andmalignantlymphocytestoimpedeanti-tumorimmunity.

简介：<正>ThesusceptibilityofprimaryBcellstoFas(APO-1,CD95)-mediatedapoptosisisregulatedbysignalsderivedfromadditionalsurfacereceptors.CD40engagementproducesupregulationofFasexpressionandinducesmarkedsensitivitytoFas-inducedcelldeath,whereasBcellantigenreceptor(BCR)engagementinhibitsFaskillingandtherebyproducesFas-resistance,eveninotherwisesusceptible,CD40-stimulatedtargets.BCRsignalingforinducibleFas-resistancedevelopsoveraperiodof12hoursanddependson

简介：被象染色体冷凝作用，面向双性人的锭子形成，染色体大会离子，分离和胞质分裂那样的一系列紧安排的事件精确通过有丝分裂调整。染色体运动被和位于着丝点以内的一个专业化染色体领域的锭子微导管的相互作用在有丝分裂期间管理。这个专业化区域，叫了kinetochore，是为锭子微导管着丝点的地点协会。除了用作在染色体和锭子微导管之间的一个物理连接，kinetochore通过微导管马达和定位在或在它附近的锭子集会检查点(囊)传感器在chromosomal分离展出一个活跃角色[例如，1]。

简介：<正>WeandothershavefirmlyestablishedthatsurfaceIgMreceptor(sIgM-R)crosslinkingwithantibodiestotheiheavychain(anti-i)leadstogrowtharrestandapoptosisinaseriesofwellcharacterizedB-celllymphomas.Thisrequiresablationofc-Mycproteinexpressionandtheconcomitantinductionofthecyclin-dependent-kinaseinhibitor,p27Kip1.Thesignalingmechanismsregulatingc-Mycandp27Kip1proteinexpressionarepoorlyunderstood.However,werecentlyestablishedthatsIgM-Rmediateddown-modulationofthePI-3Kpathwaydirectlyaffectedc-Mycandp27Kip1expressionandaccuratelypredictedgrowtharrest

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