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Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
Published on: August 21, 2017
Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology
Kazuo Fujihara1, Jeffrey L Bennett2, Jerome de Seze2
1From the Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine; and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Departments of Neurology and Ophthalmology (J.L.B.), Programs in Neuroscience and Immunology, School of Medicine, University of Colorado, Aurora; Department of Neurology (J.S.), Hôpital de Hautepierre, Strasbourg Cedex, France; Chugai Pharmaceutical Co. (M.H.), Ltd, Tokyo, Japan; Department of Neurology (I.K.), St. Josef Hospital, Ruhr University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, Berg, Germany; Department of Neurology (B.G.W.), Mayo Clinic, Rochester, MN; ApotheCom (D.K., T.M.), London, UK; and Department of Immunology (T.Y.), National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. fujikazu@med.tohoku.ac.jp.
Neuromyelitis optica spectrum disorder (NMOSD) management aims to reduce relapses. Blocking interleukin-6 (IL-6) signaling, a key factor in NMOSD, shows promise in preventing these attacks.
Area of Science:
- Neuroimmunology
- Autoimmune Disorders
- Cytokine Signaling
Background:
- Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune disease targeting the central nervous system, primarily the optic nerves and spinal cord.
- NMOSD attacks cause significant neurological disability, making relapse prevention a critical treatment goal.
- Current treatments involve immunosuppressants, but novel therapeutic targets are needed.
Purpose of the Study:
- To review the role of interleukin-6 (IL-6) in the pathophysiology of NMOSD.
- To explore the therapeutic potential of targeting the IL-6 pathway for NMOSD management.
Main Methods:
- Review of existing literature on IL-6 in NMOSD.
- Analysis of data from case series and Phase 3 randomized controlled trials on IL-6 receptor (IL-6R) inhibition.
Main Results:
- Elevated IL-6 levels are observed in NMOSD patients.
- IL-6 contributes to NMOSD pathogenesis through various mechanisms, including B-cell activation and blood-brain barrier disruption.
- IL-6R inhibition has demonstrated reduced relapse rates in NMOSD patients.
Conclusions:
- IL-6 plays a significant role in NMOSD.
- Inhibition of IL-6 activity represents a promising therapeutic strategy for managing NMOSD.
- Targeting IL-6R offers a new avenue for reducing relapse frequency and severity in NMOSD.
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