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Updated: May 26, 2025

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
Published on: August 21, 2017
Structural basis of aquaporin-4 autoantibody binding in neuromyelitis optica
Meghna Gupta1,2, Nitesh Kumar Khandelwal1,2, Andrew Nelson1
1Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.
Abstract:
Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system where pathogenic autoantibodies target the water channel aquaporin-4 on human astrocytes causing neurological impairment. Autoantibody binding leads to complement-dependent and complement-independent cytotoxicity, ultimately resulting in astrocyte death, demyelination, and neuronal loss. Aquaporin-4 assembles in astrocyte plasma membranes as symmetric tetramers or as arrays of tetramers. We report molecular structures of aquaporin-4 alone and bound to Fab fragments from patient-derived NMO autoantibodies using cryogenic electron microscopy. Each antibody binds to epitopes comprised of three extracellular loops of aquaporin-4 with contributions from multiple molecules in the assembly. The structures distinguish between antibodies that bind to the tetrameric form of aquaporin-4 and those targeting higher-order orthogonal arrays of tetramers that provide more diverse bridging epitopes.

