Dual role of Ninjurin-1 in myeloid cell adhesion and inflammation in relapse-remitting EAE

myeloid cells display both adhesion-related and inflammatory activation features, characterized by increased antigen presentation, cytokine production, and transcriptional enrichment for genes regulating adhesion, migration, and innate immune signaling. Importantly, therapeutic blockade of Ninjurin-1 reduced clinical severity, CNS immune infiltration, and demyelination in RR-EAE. These findings uncover a previously unrecognized role for Ninjurin-1 in myeloid-driven neuroinflammation and support Ninjurin-1 as a candidate therapeutic target for relapsing-remitting MS.