[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100612253":3},{"organization":4,"armGroups":7,"interventions":25,"overallOfficials":10,"centralContacts":30,"locations":37,"responsibleParty":55,"collaborators":10,"id":57,"slug":10,"hasResults":58,"nctId":59,"briefTitle":60,"officialTitle":60,"acronym":61,"eligibilityCriteria":62,"healthyVolunteers":58,"sex":63,"minAge":64,"maxAge":65,"enrollmentInfo":66,"targetDuration":10,"studyType":69,"phases":10,"briefSummary":70,"conditions":71,"keywords":10,"overallStatus":77,"whyStopped":10,"lastUpdateSubmitDate":78,"lastUpdatePostDateStruct":79,"startDateStruct":82,"completionDateStruct":84,"leadSponsor":86,"locationsCount":87},{"fullName":5,"class":6},"University Hospital, Strasbourg, France","OTHER",[8,13,16,19,22],{"label":9,"type":10,"description":10,"interventionNames":11},"Systemic lupus erythematosus",null,[12],"Biological: blood draw",{"label":14,"type":10,"description":10,"interventionNames":15},"Systemic scleroderma",[12],{"label":17,"type":10,"description":10,"interventionNames":18},"ANCA-associated vasculitis",[12],{"label":20,"type":10,"description":10,"interventionNames":21},"Antiphospholipid syndrome",[12],{"label":23,"type":10,"description":10,"interventionNames":24},"Primary immunodeficiencies",[12],[26],{"type":27,"name":28,"description":28,"armGroupLabels":29,"otherNames":10},"BIOLOGICAL","blood draw",[17,20,23,9,14],[31],{"name":32,"role":33,"phone":34,"phoneExt":35,"email":36},"Anne-Sophie KORGANOW, MD","CONTACT","03 69 55 09 94","0033","anne-sophie.korganow@chru-strasbourg.fr",[38],{"facility":39,"status":10,"city":40,"state":10,"zip":41,"country":42,"cosmosGeoPoint":43,"geoPoint":48,"contacts":49},"Hôpitaux Universitaires de Strasbourg","Strasbourg","67000","France",{"type":44,"coordinates":45},"Point",[46,47],7.74553,48.58392,{"lat":47,"lon":46},[50,52,53],{"name":32,"role":33,"phone":51,"phoneExt":35,"email":36},"+33369551123",{"name":10,"role":33,"phone":10,"phoneExt":10,"email":36},{"name":32,"role":54,"phone":10,"phoneExt":10,"email":10},"PRINCIPAL_INVESTIGATOR",{"type":56,"investigatorFullName":10,"investigatorTitle":10,"investigatorAffiliation":10,"oldNameTitle":10,"oldOrganization":10},"SPONSOR","100612253",false,"NCT07251179","Characterization of Autoreactive b Lymphocytes in Autoimmune Diseases and Immune Deficiencies","AutoB-Tetramer","Inclusion Criteria:\n\n* Patients aged between 18 and 70\n* Patients for whom at least one of the following conditions has been confirmed:\n* Systemic lupus erythematosus meeting the 2019 ACR\u002FEULAR classification criteria.\n* Systemic scleroderma meeting the 2013 ACR\u002FEULAR classification criteria. ANCA-associated vasculitis according to the 2022 EULAR\u002FACR classification criteria.\n* Antiphospholipid syndrome according to the 2023 ACR\u002FEULAR criteria.\n* Primary immunodeficiencies according to IUIS criteria.\n* Patients capable of understanding the objectives of the research.\n* Patients affiliated with a social security health insurance scheme (beneficiary or dependant).\n* Patients who have signed and dated the informed consent form for non-identifying genetic testing.\n\nExclusion Criteria:\n\n* Patient refusing to participate in the study\n* Patient in a period of exclusion (determined by a previous or ongoing study) Inability to provide the subject with informed consent (in an emergency or immediate life-threatening situation, difficulties in understanding the subject, etc.)\n* Patient under legal protection\n* Patient under guardianship or conservatorship","ALL","18 Years","70 Years",{"count":67,"type":68},200,"ESTIMATED","OBSERVATIONAL","Autoimmune diseases (AID), whether systemic or organ-specific, affect approximately one in ten people, and their prevalence continues to increase. Many AIDs are linked to the emergence of autoreactive B cells (BCs) directed against components of the self. In healthy individuals, these autoreactive B cells are counter-selected or regulated before reaching the antibody-secreting cell compartment. However, in predisposed individuals, a breakdown in B cell tolerance can occur, leading to the formation of autoantibodies with devastating consequences, such as the emergence of systemic lupus erythematosus (SLE), rheumatoid arthritis, and vasculitis. B-cell depletion is often beneficial in these patients, but paradoxically, therapies targeting B cells are not always effective. Furthermore, B cell depletion via LB-specific antibodies (anti-CD20) or treatment with CD19 chimeric antigen receptor T cells (CAR T) leads to complete and prolonged depression of the entire B compartment without targeting the LB population responsible for the onset of the disease. To date, two pitfalls in studies of human autoreactive LBs often complicate the interpretation of results:\n\ni) the difficulty of identifying autoreactive LBs among all LBs, ii) demonstrating the pathogenicity of autoreactive B lymphocytes when they can be identified individually. We propose to quantify and phenotype these autoreactive\u002Fpathogenic B cells using high-throughput flow cytometry in several clinical situations.",[72,73,74,75,76],"Systemic Lupus Erythematosus","Systemic Scleroderma","ANCA-associated Vasculitis","Antiphospholipid Syndrome","Primary Immunodeficiencies","NOT_YET_RECRUITING","2025-11-26",{"date":80,"type":81},"2025-12-04","ACTUAL",{"date":83,"type":68},"2026-01-01",{"date":85,"type":68},"2031-12-31",{"name":5,"class":6},1]