B lymphocytes in neuromyelitis optica.
2015-06-01 | journal article. A publication with affiliation to the University of Göttingen.
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B lymphocytes in neuromyelitis optica.
Bennett, J. L.; O'Connor, K. C.; Bar-Or, A.; Zamvil, S. S.; Hemmer, B.; Tedder, T. F. & von Büdingen, H.-C. et al. (2015)
Neurology® neuroimmunology & neuroinflammation, 2(3) art. e104. DOI: https://doi.org/10.1212/NXI.0000000000000104
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Details
- Authors
- Bennett, Jeffrey L.; O'Connor, Kevin C.; Bar-Or, Amit; Zamvil, Scott S.; Hemmer, Bernhard; Tedder, Thomas F.; von Büdingen, H-Christian; Stuve, Olaf; Yeaman, Michael R.; Smith, Terry J.; Stadelmann, Christine
- Abstract
- Neuromyelitis optica (NMO) is an inflammatory autoimmune disorder of the CNS that predominantly affects the spinal cord and optic nerves. A majority (approximately 75%) of patients with NMO are seropositive for autoantibodies against the astrocyte water channel aquaporin-4 (AQP4). These autoantibodies are predominantly IgG1, and considerable evidence supports their pathogenicity, presumably by binding to AQP4 on CNS astrocytes, resulting in astrocyte injury and inflammation. Convergent clinical and laboratory-based investigations have indicated that B cells play a fundamental role in NMO immunopathology. Multiple mechanisms have been hypothesized: AQP4 autoantibody production, enhanced proinflammatory B cell and plasmablast activity, aberrant B cell tolerance checkpoints, diminished B cell regulatory function, and loss of B cell anergy. Accordingly, many current off-label therapies for NMO deplete B cells or modulate their activity. Understanding the role and mechanisms whereby B cells contribute to initiation, maintenance, and propagation of disease activity is important to advancing our understanding of NMO pathogenesis and developing effective disease-specific therapies.
- Issue Date
- 1-June-2015
- Journal
- Neurology® neuroimmunology & neuroinflammation
- Organization
- Universitätsmedizin Göttingen
- ISSN
- 2332-7812
- Language
- English