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

Jeffrey L Bennett1, Kevin C O'Connor1, Amit Bar-Or1

  • 1Departments of Neurology and Ophthalmology and Neuroscience Program (J.L.B.), University of Colorado, Denver; Department of Neurology (K.C.O.), Yale University School of Medicine, New Haven, CT; Neuroimmunology Unit (A.B.-O.), Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada; Department of Neurology (S.S.Z., H.-C.v.B.), UCSF School of Medicine, San Francisco, CA; Department of Neurology (B.H.), Technische Universität München, Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Department of Immunology (T.F.T.), Duke University Medical Center, Durham, NC; Departments of Neurology and Neurotherapeutics (O.S.), University of Texas Southwestern Medical Center, Dallas, TX; Department of Medicine (M.R.Y.), Divisions of Molecular Medicine and Infectious Diseases, University of California, Los Angeles; Harbor-UCLA Medical Center (M.R.Y.), Torrance, CA; Departments of Ophthalmology and Visual Sciences and Internal Medicine (T.J.S.), University of Michigan Medical School, Ann Arbor; and Institute of Neuropathology (C.S.), University Medical Center, Göttingen, Germany.

Neurology(R) Neuroimmunology & Neuroinflammation
|May 16, 2015
PubMed
Summary

Neuromyelitis optica (NMO) involves CNS inflammation, often linked to aquaporin-4 (AQP4) autoantibodies. B cells are crucial in NMO pathogenesis, driving disease through various immune mechanisms.

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Area of Science:

  • Neuroimmunology
  • Autoimmune Disorders
  • Central Nervous System (CNS) Inflammation

Background:

  • Neuromyelitis optica (NMO) is a severe inflammatory autoimmune disorder of the CNS.
  • It primarily affects the spinal cord and optic nerves.
  • Most NMO patients (approx. 75%) have autoantibodies against aquaporin-4 (AQP4), predominantly IgG1, which are pathogenic and cause astrocyte injury.

Purpose of the Study:

  • To elucidate the fundamental role of B cells in NMO immunopathology.
  • To understand the diverse mechanisms by which B cells contribute to NMO initiation, maintenance, and propagation.
  • To inform the development of effective, disease-specific therapies for NMO.

Main Methods:

  • Review of clinical and laboratory-based investigations.
  • Analysis of hypothesized B cell mechanisms in NMO pathogenesis.
  • Examination of current therapeutic strategies targeting B cells in NMO.

Main Results:

  • B cells play a fundamental role in NMO immunopathology.
  • Hypothesized mechanisms include AQP4 autoantibody production, enhanced B cell/plasmablast activity, and dysregulation of B cell tolerance and function.
  • Current therapies often target B cell depletion or modulation.

Conclusions:

  • Understanding B cell mechanisms is critical for advancing NMO pathogenesis knowledge.
  • Targeting B cell pathways offers potential for developing novel NMO treatments.
  • Further research into B cell roles will guide future therapeutic strategies.