Humoral immune responses mediate peripheral nerve damage and represent important pharmacological targets in chronic inflammatory demyelinating polyneuropathy (CIDP), the most common treatable acquired chronic polyneuropathy. IgG Fc-linked glycan structures determine antibody-mediated effector functions and were identified as a molecular switch shifting IgG activity from a pro-inflammatory to an anti-inflammatory pathway. We demonstrate that patients with CIDP show higher levels of IgG-Fc N-glycans lacking terminal galactose and sialic acid residues as compared to demographically matched healthy individuals. Furthermore, longitudinal analysis of two independent CIDP patient cohorts revealed that changes in IgG-Fc glycan composition, in particular the addition of terminal sialic acid, are associated with clinical improvement. Our findings suggest that the clinical response in CIDP patients could be potentially enhanced by Fc-glycan modification induced by immunotherapies.