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

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