Core Viewpoint - The study highlights the pathogenic role of meningeal B cells in driving neuroinflammation relapses in central nervous system autoimmune diseases, particularly multiple sclerosis (MS) [2][6]. Group 1: Research Findings - Meningeal autoreactive B cells interact with antigen-specific T cells, accelerating neuroinflammation [3][6]. - In an experimental autoimmune encephalomyelitis (EAE) mouse model, meningeal autoreactive B cells amplify local pro-inflammatory mechanisms through their interaction with T cells, promoting neutrophil recruitment and endothelial cell activation prior to clinical disease onset [4][6]. - The mechanism requires B cells to express major histocompatibility complex class II (MHC II) molecules and T cells to produce granulocyte-macrophage colony-stimulating factor (GM-CSF) [5]. Group 2: Implications for Treatment - The findings confirm that local autoreactive B cells in the brain are key initiators of neuroinflammation in relapsing MS and represent promising therapeutic targets [6][7]. - Selective depletion of brain-resident B cells can alleviate relapses in experimental autoimmune encephalomyelitis [7].