our study provides an integrated multi-omics characterization of compartment-specific B-cell N-glycosylation remodeling in anti-NMDAR encephalitis. By combining CSF IgG glycoproteomics with paired single-cell transcriptomics, we identify a coordinated transcriptional reprogramming associated with inflammatory microenvironmental signaling, B-cell differentiation, and altered Fc glycan composition. Importantly, our findings support a model in which increasing antibody biosynthetic demand progressively exceeds the relative capacity for terminal glycan processing during plasma-cell activation, providing a plausible explanation for the discordance between glycosyltransferase transcription and the under-sialylated IgG phenotype observed in poor outcome groups.