简介：TcellhomeostasiscommonlyreferstothemaintenanceofrelativelystableTcellnumbersintheperipherallymphoidorgans.AmongthelargenumbersofTcellsintheperiphery,Tcellsexhibitstructuraldiversity,I.e.,theexpressionofadiverserepertoireofTcellreceptors(TCRs),andfunctionaldiversity,I.e.,thepresenceofTcellsatna(I)ve,effector,andmemorydevelopmentalstages.AlthoughthehomeostasisofTcellnumbershasbeenextensivelystudied,investigationofthemechanismsunderlyingthemaintenanceofstructuralandfunctionaldiversityofTcellsisstillatanearlystage.ThefundamentalfeaturethroughoutTcelldevelopmentistheinteractionbetweentheTCRandeitherselforforeignpeptidesinassociationwithMHCmolecules.Inthisreview,wepresentevidenceshowingthathomeostasisofTcellnumberanddiversityismediatedthroughcompetitionforlimitingresources.ThenumberofTcellsismaintainedthroughcompetitionforlimitingcytokines,whereasthediversityofTcellsismaintainedbycompetitionforself-peptide-MHCcomplexes.Inotherwords,diversityoftheself-peptiderepertoirelimitsthestructural(TCR)diversityofaTcellpopulation.Wespeculatethatcognatelowaffinityself-peptides,actingasweakagonistsandantagonists,regulatethehomeostasisofTcelldiversitywhereasnon-cognateornullpeptideswhichareextremelyabundantforanygivenTCR,maycontributetothehomeostasisofTcellnumberbyprovidingsurvivalsignals.Moreover,self-peptidesandcytokinesmayformspecializednichesfortheregulationofTcellhomeostasis.

简介：<正>Apoptosisisahighlyregulatedphysiologicalprocesscriticalindevelopmentandtissuehomeostasis.Abnormalapoptosiscanleadtodiseaseconditionsincludingneurodegeneration,autoimmunityandcancer.DNAfragmentationisanintegralpartofapoptosisandhaslongbeensuspectedtobeofcriticalimportanceincleaninguppotentiallyantigenicDNAandgeneticmaterialcapableofinducingneoplasmictransformationinneighboringcells.DirectevidenceforthisfunctionofDNAfragmentationhowever,isstilllacking.TheidentificationofaheterodimericDNAfragmentationfactor45and40(DFF45andDFF40,alsocalledICADforInhibitorofCaspaseActivatedDNaseandCADforCaspaseActivatedDNaserespectively)aswellas

简介：AbstractIntestinal homeostasis depends on complex interactions between the gut microbiota and host immune system. Emerging evidence indicates that the intestinal microbiota is a key player in autoimmune liver disease (AILD). Autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, and IgG4-related sclerosing cholangitis have been linked to gut dysbiosis. Diverse mechanisms contribute to disturbances in intestinal homeostasis in AILD. Bacterial translocation and molecular mimicry can lead to hepatic inflammation and immune activation. Additionally, the gut and liver are continuously exposed to microbial metabolic products, mediating variable effects on liver immune pathologies. Importantly, microbiota-specific or associated immune responses, either hepatic or systemic, are abnormal in AILD. Comprehensive knowledge about host-microbiota interactions, included but not limited to this review, facilitates novel clinical practice from a microbiome-based perspective. However, many challenges and controversies remain in the microbiota field of AILD, and there is an urgent need for future investigations.

简介：Eachcomponentofthehumanearperformsaspecificfunctioninhearing.Theactualprocessofsoundtransductiontakesplaceintheauditoryportionoftheinnerear,thefluid-filledcochlea.Inthecochlea,thesensitivityandefficiencyofsensoryapparatustoconvertmechanicalenergyintoneuralactivity,largelydependsonthefluidicandionicenvironment.Inthelateralwallofcochlea,thesecretoryepitheliumstriavascularisplaysanimportantroleinthemaintenanceoffluidicandionichomeostasis.Avarietyofgenemutationsdisturbsthecochlearhomeostasisandsubsequentlyleadstohearingimpairment.Thereviewcoversseveralaspectsofcochlearhomeostasis,fromcochlearfluidandthefunctionalroleofstriavascularis,cochlearK+recyclinganditsmolecularsubstratestogeneticdeafnesswithabnormalcochlearhomeostasis.

简介：当一个非免疫学的机关首先从事了新陈代谢的、滋养的存储和detoxification活动，人的肝通常被察觉。然而，我们现在知道健康的肝也是复杂免疫学的一个地点活动象非造血的房间人口一样由一个多样的有免疫力的房间全部剧目调停了。在疾病得非的肝，新陈代谢并且织物改变功能要求发炎的元素。在有到饮食、微生物引起的产品的常规暴露的联合，这发炎为过多的有免疫力的激活创造潜力。在这复杂微型环境，肝的免疫系统容忍无害的分子当同时对可能的传染代理人仍然保持警惕时，恶意的房间或纸巾损坏。在到由病原体或织物损坏的挑战的适当有免疫力的激活之上，解决发炎的机制是必要的维持肝动态平衡。清除‘的失败；dangerous’；刺激或调整适当地激活的有免疫力的机制导致病理学的发炎和纤维变性，肝硬化和最终的肝失败的进步发展描绘的破坏织物动态平衡。肝的煽动性的机制因此在健康的成年的肝有角色的一个系列；他们是必要的维持织物和机关动态平衡并且dysregulated，肝病理的关键司机与长期的感染，autoimmunity和恶意被联系。在这评论，我们在正常的肝动态平衡探索发炎和煽动性的调停人的变化感觉并且求婚作为一条治疗学的途径肝特定的有免疫力的规定小径指向治疗肝疾病。

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简介：Despitethefactthatironisoneofthemostabundantelementsoftheearth'scrust,irondeficienciesareseriousproblemsbothinhumannutrition[1]andinagriculture[2].Sixtoeightpercentoftheworld'spopulationispotentiallyaffectedbyirondeficiencyinducedanemia,aleadingcauseofmaternaldeathinAfricanandAsiancountrieswherepeoplerelymostlyonplantsfortheirdailyintakeofiron.Ironcanalsobealimitingfactorinthegrowthofeconomicallyimportantcropplantsbecauseofinadequatesoilchemistry,andsuchdeficienciescannoteasilybecorrectedbyamendingthesoil.Improvingtheplant'sabilitytoabsorbironinadverseconditionsandtoincreasetheiroverallcontentcouldoffersolutionstothesedramaticproblems.Thereforeunderstandingthemolecularmechanismsregulatingironuptakeandhomeostasisinplantshaspotentiallyimportantpracticalapplicationsbothinagricultureandhumanhealth[3].

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简介：ＴＢｕｒｎＲｅｓｅａｒｃｈＩｎｓｔｉｔｕｔｅ，ＳｏｕｔｈｗｅｓｔｅｒｎＨｏｓｐｉｔａｌ，ＴｈｉｒｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＣｏｌｅｇｅ，Ｃｈｏｎｇｑｉｎｇ４０００３８，Ｃｈｉｎａ（ＣｈｉＬＸ，ＹａｎｇＺＣ，ＷａｎｇＸａｎｄＬｉＡ）Ｔｈｉｓｓｔ...

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简介：Interleukin-15(IL-15)为记忆CD8+和CD4+T的幸存是必要的房间子集，和天赋漂亮、自然的漂亮T房间。这里，我们描述一迄今在调整天真的CD4+T房间的homoeostasis的IL-15的unreported角色。从非肥胖的糖尿病患者(点头)的splenocytes的采纳转移在在lymphopenicNOD.scid.Il15−/−老鼠的T房间的增加的homeostatic扩大的老鼠结果什么时候与NOD.scid接受者相比。CD4+T房间的增加的累积也在NOD.Il15−/−老鼠被观察，显示那条IL-15-dependent规定也当淋巴球减少症不在时发生。缺乏IL-15Rα的NOD.scid老鼠；锁住，然而并非缺乏普通gamma的那些也锁住表演CD4+T房间的增加的累积。这些调查结果显示IL-15-mediated规定在CD4+T房间上直接发生并且要求IL-15的trans演讲。当IL-15不在时膨胀发信号的CD4+T房间不获得古典规章的T房间的特征。更确切地说，当IL-15表演不在时膨胀的CD4+T房间损害了导致抗原的激活和IFN-γ；生产。把调查结果基于这些，我们建议天真的CD4+T房间分隔空间的IL-15-dependent规定可以代表控制的另外的层潜在地阻挠逃离中央忍耐的autoreactive房间，当允许记忆T房间的扩大时。

简介：Heatshockprotein70(HSP70)maintainsCa~(2+)homeostasisinPC12cells,whichmayprotectagainstapoptosis;however,themechanismsofneuroprotectionareunclear.Therefore,inthisstudy,weexaminedCa~(2+)levelsinPC12cellstransfectedwithanexogenouslentiviralHSP70geneexpressionconstruct,andwesubsequentlysubjectedthecellstoischemia-hypoxia/reoxygenationinjury.HSP70overexpressionincreasedneuronalviabilityandATPaseactivity,anditdecreasedcellularreactiveoxygenspecieslevelsandintracellularCa~(2+)concentrationafterhypoxia/reoxygenation.HSP70overexpressionenhancedtheproteinandmRNAexpressionlevelsofsarcoplasmic/endoplasmicreticulumCa~(2+)-ATPase(SERCA),butitdecreasedtheproteinandmRNAlevelsofinositol1,4,5-trisphosphatereceptor(IP3R),therebyleadingtodecreasedintracellularCa~(2+)concentrationafterischemia-hypoxia/reoxygenation.TheseresultssuggestthatexogenousHSP70protectsagainstischemia-hypoxia/reoxygenationinjury,atleastinpart,bymaintainingcellularCa~(2+)homeostasis,byupregulatingSERCAexpressionandbydownregulatingIP_3Rexpression.

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