Website：Info：Westudyhowimmunecellsgoawryinpediatricinflammatory，allergic，autoimmuneandautoinflammatoryconditions。Westrivetoidentifykeypathogenicmechanismsanddevelopnoveldiagnosticandtreatmentmethodsthatmayimprovethequalityoflifeinchildren。Cutting-edgetechnologies，includingdisease-causalandriskgeneidentification，single-cellbaseddiseasetissueprofiling，andmechanisticexplorationusingbioinformatic，biochemical，immunologicalandanimalmodelstudies，haveshapedourapproachinhelpingtheclinicianstoachievepersonalizeddiagnosisandpathogenesis-basedtreatmentpractice。Funding：2016-2019：GuangzhouWomenandChildren’sMedicalCentreStart-upFund（YuxiaZhang）2018-2020：NationalNaturalScienceFoundationofChina（91742109，YuxiaZhang）2018-2021：NationalNaturalScienceFoundationofChina（31770978，YuxiaZhang）2019-2022：NaturalScienceFoundationofChina（91842304，JunWang，BingtaiLu）2019-2022：NationalNaturalScienceFoundationofChina（81901655，MengLin）Keypublications：MucosalProfilingofPediatric-OnsetColitisandIBDRevealsCommonPathogenicandTherapeuticPathways，Cell（2019），Https：//doi.org/10.1016/j.cell.2019.10.027IncollaborationwithGastroenterologyDepartmentofGWCMCandPekingUniversity，weperformedsingle-cellandriskgeneanalysisofchildrenwithundifferentiatedcolitis，Crohn’sdiseaseandulcerativecolitis。ThishasidentifiedthatacommonunderlyingmechanismofpathogenesisisthedefectivecAMPsignaling，whichresultsinCD39+intraepithelialTcell（CD39+IET）deficiency，macrophagehyperinflammationandplateletaggregationatthecolonicmucosae。Thisstudyhasledtoasuccessfulpilottrialusingapan-phosphodiesteraseinhibitordipyridamoleforthetreatmentofchildrenwithcolitis。Trialregistrationcanbefoundathttp：//www.chictr.org.cn/showprojen.aspx？proj=25986Cordbloodmonocyte-derivedinflammatorycytokinessuppressIL-2andinducenonclassic"T（H）2-type"immunityassociatedwithdevelopmentoffoodallergy，SciTranslMed。2016Jan13；8（321）：321ra8。doi：10.1126/scitranslmed.aad4322。CordBloodCD8+TCellsHaveaNaturalPropensitytoExpressIL-4inaFattyAcidMetabolismandCaspaseActivation-DependentManner，FrontImmunol。2018Apr25；9：879。doi：10.3389/fimmu.2018.00879。eCollection2018。IncollaborationwiththeBarwonInfantStudyandtheWalter&ElizaHallInstituteofMedicalResearch，weidentifythathyper-inflammationatbirthisakeypathogenicmechanismthatmayleadtoIgE-mediatedfoodallergy（SciTranslMed）andchroniccolitis（FrontImmunol）inchildren。AutoinflammatorymutationinNLRC4revealsaleucine-richrepeat（LRR）-LRRoligomerizationinterface，JAllergyClinImmunol。2018Dec;142（6）：1956-1967.e6。doi：10.1016/j.jaci.2018.04.033。Epub2018May17。IncollaborationwithImmunologyDepartmentofGWCMCandtheWalter&ElizaHallInstituteofMedicalResearch，weidentifiedanovelmutationintheinflammasomeproteinNLRC4，whichhasproventocausemacrophageactivationsyndromewithcomplexclinicalpresentations。Labmembers：PI：YuxiaZHANG张玉霞Co-PI：JunWANG王俊Postdoctoratefellows：BingtaiLU，卢秉泰MingLIU，刘明BingHUANG，黄冰HuifangXIAN，冼惠芳MengLIN，林萌ZhiyaoZHAO，赵芝瑶YanhuiXU，徐艳慧ResearchAssistant：LiZHANG，张莉HanqingWANG，王寒晴CaiqinGUO，郭彩琴WanmingHUANG，黄婉明JunliNIE，聂君礼RongzeWANG，王荣泽Students：ShanmeiziZHAO，赵山美子XuanjieGUO，郭玄杰RongliFANG，方榕丽YuxiaZhang，PH.DGuangzhouWomenandChildren’sMedicalCenterGuangzhouMedicalUniversityGuangzhou，510623，ChinaEmail：yuxia.zhang@zhanglaboratory.comWebpage：zhanglaboratory.comResearchbackground：YuxiaobtainedherPhDfromtheChineseAcademyofSciencesin2007，followedby2yearspost-doctoraltrainingintheChristopherRuddLaboratoryattheUniversityofCambridge（UK）（2007-2008）。ShejoinedtheLeonardHarrisonLabatWalterandElizaHallInstituteofMedicalResearch（WEHI）inFebruary2009andwaspromotedtoSeniorResearchOfficerin2014。ShewasappointedLabHeadApril2016atGuangzhouWomenandChildren’sMedicalcenter（GWCMC），GuangzhouMedicalUniversity。Shebridgesmouseandhumanimmunologystudieswithcutting-edgeepigenetic，metabolomicandcellsignalingmethodologies，andhasidentifiednovelbiomarkersandpathogenicmechanismsinautoimmuneandallergicdiseases，andtherapeutictargetsandagents。Herlabcurrentlyfocusesonimmunepathogenesisandnoveltreatmentstrategiesforinflammatoryboweldiseases（IBD）andbiliaryatresia（BA）.Theyemploycutting-edgetechniquesincludingsinglecellRNAsequencing，wholegenome-wideassociationstudy，wholeexosomesequencing，comparativeimmuneprofiling，animalexperimentsandclinicaltrialstoidentifyhowriskanddiseasecausalgenesregulateintestinalandhepaticimmuneandnon-immunecelldevelopmentandfunction。张玉霞于2007年获得中国科学院大学博士学位，随后在英国剑桥大学接受了两年的博士后培训（2007-2008）。2009年2月，她加入了沃尔特•伊丽莎•霍尔医学研究所（WEHI），并于2014年晋升为高级研究官员。2016年4月，她受邀在广州医科大学广州妇女儿童医疗中心组建实验室。她通过免疫学、遗传学、表观遗传学、代谢组学和细胞信号传导等的交叉学科方法将小鼠和人类免疫学研究联系起来，发现了自身免疫性和过敏性疾病中的新的生物标志物和致病机制，以及治疗靶点和药物。她的实验室目前专注于儿童消化系统慢病的免疫发病机制和新的治疗策略研究。他们采用包括单细胞RNA转录组测序、全基因组关联研究、全外显现子测序、比较免疫图谱、动物实验和临床试验的方法，确定疾病的风险和致病基因如何调节组织器官的功能稳态。Educationandemployment1）1997-2001ShenyangPharmaceuticalUniversity，Shenyang，China。Bachelor’sinpharmaceuticalmedicine2）2001-2002BeijingKaiwenBiotechLtd，BeijingChina。QualityControlofficer3）2002-2007UniversityofChineseAcademyofSciences，Beijing，China。PH.Dinvirologyandmolecularimmunology。Supervisor，PoTien4）2007-2009UniversityofCambridge，Cambridge，UK。ResearchAssociate，SupervisorProf.ChristopherERudd5）2009-2016WalterandElizaHallInstituteofMedicineResearch，Parkville，Australia。SeniorResearchOfficer，SupervisorProf。LeonardHarrison6）2016-CurrentGuangzhouWomenandChildren’sMedicalCenter，GuangzhouUniversity。PrincipalInvestigator，ProfessorFunding：1）2018-2020NSFC，Projectgrant（91742109）600，000CNYPI2）2018-2021NSFC，Projectgrant（31770978）600，000CNYPI3）2017-2020NHMRC（APP1129033）$452，298CIB4）2014-2018NHMRC（APP1082307）$833，257.10CID5）2013-2015WEHICatalystFund$38，410CIA6）2013-2016JDRF（17-2013-547）$497，724CIB7）2011-2013WEHIGenomicsFund$34，299CIA8）2010-2012JDRFPostdocFellowship（3-2010-448）$100，364TeachingandSupervising：Current：7postdocs，1PH.Dcandidate（co-supervising），3Mastercandidates，6RAPast：twoPH.Dstudents（co-supervisor），JulinBosco，YanhuiXu（MelbourneUniversity）Patents：1）MethodoftreatingsepsisbyadministeringasolubleCD52glycoprotein，USPatent9，585，9692）Solublemediator，USPatent9，585，969Representativepublications：[1-15]1、Xian，H。，etal。，LRRC59modulatestypeIinterferonsignalingbyrestrainingtheSQSTM1/p62-mediatedautophagicdegradationofpatternrecognitionreceptorDDX58/RIG-I。Autophagy，2019：p。1-11。2、Huang，B。，etal。，MucosalProfilingofPediatric-OnsetColitisandIBDRevealsCommonPathogenicsandTherapeuticPathways。Cell，2019。179（5）：p。1160-1176e24。3、Zhang，Y。，etal。，CordBloodCD8（+）TCellsHaveaNaturalPropensitytoExpressIL-4inaFattyAcidMetabolismandCaspaseActivation-DependentManner。FrontImmunol，2018。9：p。879。4、Rashidi，M。，etal。，CD52inhibitsToll-likereceptoractivationofNF-kappaBandtriggersapoptosistosuppressinflammation。CellDeathDiffer，2018。25（2）：p。392-405。5、Moghaddas，F。，etal。，AutoinflammatorymutationinNLRC4revealsaleucine-richrepeat（LRR）-LRRoligomerizationinterface。JAllergyClinImmunol，2018。6、Zhang，Y。andB。Huang，TheDevelopmentandDiversityofILCs，NKCellsandTheirRelevanceinHealthandDiseases。AdvExpMedBiol，2017。1024：p。225-244。7、Zhan，Y。，etal。，LifeandDeathofActivatedTCells：HowAreTheyDifferentfromNaiveTCells？FrontImmunol，2017。8：p。1809。8、Zhang，Y。，etal。，MicroRNAsinCD4（+）TcellsubsetsaremarkersofdiseaseriskandTcelldysfunctioninindividualsatriskfortype1diabetes。JAutoimmun，2016。68：p。52-61。9、Zhang，Y。，etal。，Cordbloodmonocyte-derivedinflammatorycytokinessuppressIL-2andinducenonclassic"T（H）2-type"immunityassociatedwithdevelopmentoffoodallergy。SciTranslMed，2016。8（321）：p。321ra8。10、Suaini，N.H。，etal。，ImmuneModulationbyVitaminDandItsRelevancetoFoodAllergy。Nutrients，2015。7（8）：p。6088-108。11、Zhang，Y。，etal。，Thepolycombrepressivecomplex2governslifeanddeathofperipheralTcells。Blood，2014。124（5）：p。737-49。12、Zhang，Y。，etal。，Genome-wideDNAmethylationanalysisidentifieshypomethylatedgenesregulatedbyFOXP3inhumanregulatoryTcells。Blood，2013。122（16）：p。2823-36。13、Bandala-Sanchez，E。，etal。，TcellregulationmediatedbyinteractionofsolubleCD52withtheinhibitoryreceptorSiglec-10。NatImmunol，2013。14（7）：p。741-8。14、Zhang，Y。，E。Bandala-Sanchez，andL.C。Harrison，RevisitingregulatoryTcellsintype1diabetes。CurrOpinEndocrinolDiabetesObes，2012。19（4）：p。271-8。15、Zhan，Y。，etal。，DefectsintheBcl-2-regulatedapoptoticpathwayleadtopreferentialincreaseofCD25lowFoxp3+anergicCD4+Tcells。JImmunol，2011。187（4）：p。1566-77。