[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100652606":3},{"organization":4,"armGroups":7,"interventions":10,"overallOfficials":10,"centralContacts":12,"locations":10,"responsibleParty":18,"collaborators":10,"id":22,"slug":23,"hasResults":24,"nctId":25,"briefTitle":26,"officialTitle":26,"acronym":10,"eligibilityCriteria":27,"healthyVolunteers":28,"sex":29,"minAge":30,"maxAge":31,"enrollmentInfo":32,"targetDuration":10,"studyType":35,"phases":10,"briefSummary":36,"conditions":37,"keywords":39,"overallStatus":44,"whyStopped":10,"lastUpdateSubmitDate":45,"lastUpdatePostDateStruct":46,"startDateStruct":49,"completionDateStruct":51,"leadSponsor":53,"locationsCount":10},{"fullName":5,"class":6},"Beijing Municipal Administration of Hospitals","OTHER_GOV",[8],{"label":9,"type":10,"description":11,"interventionNames":10},"Peripheral Blood Donors",null,"HLA-A11+ healthy donors or patients with chronic HBV infection will provide peripheral blood for isolation of CD8+ T cells. No study intervention will be assigned or administered to the participants. The isolated CD8+ T cells will be used for ex vivo TCR-T cell generation and subsequent functional evaluation.",[13],{"name":14,"role":15,"phone":16,"phoneExt":10,"email":17},"Minghui Li","CONTACT","010-84322078","wuhm2000@sina.com",{"type":19,"investigatorFullName":14,"investigatorTitle":20,"investigatorAffiliation":21,"oldNameTitle":10,"oldOrganization":10},"PRINCIPAL_INVESTIGATOR","Professor of Medicine","Beijing Ditan Hospital","100652606","targeting-ankrd11-reverses-hbv-specific-cd8-t-cell-dysfunction-and-tolerance-100652606",false,"NCT07777250","Targeting ANKRD11 Reverses HBV-Specific CD8+ T Cell Dysfunction and Tolerance","Inclusion Criteria:\n\n* HLA-A11+ healthy donors or patients with chronic HBV infection.\n\nExclusion Criteria:\n\n* Not HLA-A11 positive or not meeting the criteria for the designated study population；",true,"ALL","18 Years","65 Years",{"count":33,"type":34},3,"ESTIMATED","OBSERVATIONAL","Achieving a functional cure for chronic hepatitis B (CHB) is largely hindered by the irreversible functional exhaustion and immune tolerance of hepatitis B virus (HBV)-specific CD8+ T cells. In our previous studies, an in vivo CRISPR screen identified ANKRD11 for the first time as an \"epigenetic brake\" on CD8+ T-cell effector function. Loss of ANKRD11 markedly enhanced the expansion, effector function, and viral clearance capacity of HBV-specific T cells. Based on these findings, we hypothesize that ANKRD11 regulates the epigenetic program of T-cell exhaustion by restricting the activity of AP-1 family transcription factors, and that targeting ANKRD11 can reverse T-cell dysfunction and overcome immune tolerance.\n\nThis project will: (1) elucidate the epigenetic mechanisms by which ANKRD11 regulates T-cell exhaustion using conditional knockout mouse models and multi-omics approaches; (2) evaluate how ANKRD11 deficiency reshapes the differentiation trajectory and antiviral function of HBV-specific T cells in models of chronic HBV infection; and (3) develop a combinatorial gene-editing strategy integrating \"release of the brake\" with \"stepping on the accelerator\" to generate enhanced TCR-T cells and evaluate their efficacy and safety in humanized mouse models.The study is expected to define a novel mechanism by which ANKRD11 regulates T-cell exhaustion, establish an enhanced TCR-T therapeutic strategy, and provide a potential approach toward achieving a functional cure for chronic HBV infection.",[38],"Chronic Hepatitis B",[38,40,41,42,43],"CD8+ T Cell Exhaustion","ANKRD11","Epigenetic Regulation","TCR-T Cell Therapy","NOT_YET_RECRUITING","2026-08-17",{"date":47,"type":48},"2026-08-20","ACTUAL",{"date":50,"type":34},"2026-12",{"date":52,"type":34},"2028-08",{"name":5,"class":6}]