在多发性硬化症中用frexalimab抑制CD40L

Patrick Vermersch¹, Cristina Granziera¹, Yang Mao-Draayer¹+11

• ¹From the University of Lille, INSERM Unité 1172, Lille Neuroscience and Cognition, Lille University Hospital, University Hospital Federation Precise, Lille (P.V.), and Sanofi, Chilly-Mazarin (S.S., R.B., P.T.) - both in France; Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, and the Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel and University of Basel, Basel, Switzerland (C.G.); the Department of Neurology, Autoimmunity Center of Excellence, University of Michigan Medical Center, Ann Arbor, and the Michigan Institute for Neurological Disorders, Farmington Hills (Y.M.-D.); the Department of Biostatistics, University of Alabama at Birmingham School of Public Health, Birmingham (G.C.); the Department of Neurology, Dnipro State Medical University, Dnipro, Ukraine (O.K.); the Clinic of Neurology and Sleep Medicine, Acibadem City Clinic University Hospital Tokuda, Sofia, Bulgaria (I.S.); the First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic (M.D.); Sanofi, Cambridge, MA (B.D., E.W.); and Queen Mary University of London, London (G.G.).