AQP4 and neuromyelitis optica: Importantly, the pathogenic impact of IgG Fc glycosylation has been demonstrated mechanistically with human IgG: anti-aquaporin-4 autoantibodies from patients with neuromyelitis optica (NMO) induce NMO-like lesions in mouse transfer models [29, 30], and this pathogenic effect of NMO-Ig is abrogated by deglycosylation before transfer [31].