DICAM promotes T <sub>H</sub> 17 lymphocyte trafficking across the blood-brain barrier during autoimmune neuroinflammation
Marc Charabati, Camille Grasmuck, Soufiane Ghannam, Lyne Bourbonnière, Antoine Fournier, Marc‐André Lécuyer, Olivier Tastet, Hania Kébir, Rose‐Marie Rébillard, Chloé Hoornaert, Elizabeth Gowing, Sandra Larouche, Olivier Fortin, Camille L. Pittet, Ali Filali‐Mouhim, Boaz Lahav, Robert Moumdjian, Alain Bouthillier, Marc Girard, Pierre Duquette, Romain Cayrol, Evelyn Peelen, Francisco J. Quintana, Jack P. Antel, Alexander Flügel, Catherine Larochelle, Nathalie Arbour, Stéphanie Zandee, Alexandre Prat
Abstract
17 cell trafficking across the blood-brain barrier in vitro and in vivo, and alleviated disease symptoms in four distinct murine autoimmune encephalomyelitis models, including relapsing-remitting and progressive disease models. Collectively, our data highlight DICAM as a candidate therapeutic target to impede the migration of disease-inducing leukocytes into the CNS in both RRMS and PMS and suggest that blocking DICAM with a monoclonal antibody may be a promising therapeutic approach.