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Related Experiment Video

Updated: May 12, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Optic neuritis in neuromyelitis optica.

Marc H Levin1, Jeffrey L Bennett, A S Verkman

  • 1Department of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Progress in Retinal and Eye Research
|April 3, 2013
PubMed
Summary

Neuromyelitis optica (NMO) is an autoimmune disease targeting aquaporin-4 (AQP4) on astrocytes. Autoantibodies (AQP4-IgG) cause inflammation and demyelination, leading to vision loss and paralysis.

Keywords:
ADCCAQP4Aquaporin-4BBBCDCCDCCCSFCxDevic's diseaseEAEGFAPIVMPMRIMSNKNMONMOSDNeuroinflammationOAPOCTONOptic nervePERNFLTMantibody-dependent cell-mediated cytotoxicityaquaporin-4blood–brain barriercerebral spinal fluidcomplement-dependent cell-mediated cytotoxicitycomplement-dependent cytotoxicityconnexinexperimental autoimmune encephalomyelitisglial fibrillary acidic proteinintravenous methylprednisonemagnetic resonance imagingmultiple sclerosisnatural killerneuromyelitis opticaneuromyelitis optica spectrum disorderoptic neuritisoptical coherence tomographyorthogonal arrays of particlesplasma exchangeretinal nerve fiber layertransverse myelitis

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Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
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Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

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Last Updated: May 12, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

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Published on: August 21, 2017

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
12:23

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

Area of Science:

  • Neuroimmunology
  • Cellular biology
  • Pathogenesis of autoimmune disorders

Background:

  • Neuromyelitis optica (NMO) is a severe autoimmune demyelinating disease characterized by optic neuritis and transverse myelitis.
  • The identification of autoantibodies targeting aquaporin-4 (AQP4-IgG) has been crucial in understanding NMO pathogenesis.
  • AQP4 is a water channel protein critical for astrocyte function and is a primary target in NMO.

Purpose of the Study:

  • To elucidate the role of AQP4-IgG in the pathogenesis of NMO.
  • To describe the pathological features of NMO at the cellular and molecular level.
  • To review current and emerging therapeutic strategies for NMO.

Main Methods:

  • Review of existing literature on NMO, AQP4, and AQP4-IgG.
  • Analysis of pathological findings in NMO, including immune cell infiltration and demyelination.
  • Examination of the mechanisms by which AQP4-IgG triggers inflammatory responses.

Main Results:

  • AQP4-IgG binding to AQP4 on astrocytes initiates complement-dependent and antibody-dependent cytotoxicity.
  • Pathological hallmarks include perivascular immunoglobulin deposition, complement activation, astrocytic AQP4 loss, and inflammatory cell infiltration.
  • Demyelination and axon loss are key features leading to neurological deficits.

Conclusions:

  • AQP4-IgG plays a causative role in NMO pathogenesis by targeting astrocytic AQP4.
  • Current therapies include immunosuppression and plasma exchange, with novel targeted treatments under development.
  • Further research is needed to understand optic nerve vulnerability and improve NMO therapies for vision preservation.