AQP4 and neuromyelitis optica: Passive transfer of purified patient NMO IgG fractions, as well as recombinant human anti-AQP4 IgG, produces key aspects of NMO-like CNS lesion pathology, including loss of AQP4 expression, myelin breakdown, axonal injury, extensive inflammatory cell infiltration, astrocyte depletion, and neuronal cytotoxicity in a complement-dependent manner [7, 11, 88].