Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology

Neurol Neuroimmunol Neuroinflamm. 2020 Aug 20;7(5):e841. doi: 10.1212/NXI.0000000000000841. Print 2020 Sep 3.

Abstract

Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune disorder that preferentially affects the spinal cord and optic nerve. Most patients with NMOSD experience severe relapses that lead to permanent neurologic disability; therefore, limiting frequency and severity of these attacks is the primary goal of disease management. Currently, patients are treated with immunosuppressants. Interleukin-6 (IL-6) is a pleiotropic cytokine that is significantly elevated in the serum and the CSF of patients with NMOSD. IL-6 may have multiple roles in NMOSD pathophysiology by promoting plasmablast survival, stimulating the production of antibodies against aquaporin-4, disrupting blood-brain barrier integrity and functionality, and enhancing proinflammatory T-lymphocyte differentiation and activation. Case series have shown decreased relapse rates following IL-6 receptor (IL-6R) blockade in patients with NMOSD, and 2 recent phase 3 randomized controlled trials confirmed that IL-6R inhibition reduces the risk of relapses in NMOSD. As such, inhibition of IL-6 activity represents a promising emerging therapy for the management of NMOSD manifestations. In this review, we summarize the role of IL-6 in the context of NMOSD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Humans
  • Interleukin-6* / immunology
  • Interleukin-6* / metabolism
  • Neuromyelitis Optica* / drug therapy
  • Neuromyelitis Optica* / immunology
  • Neuromyelitis Optica* / metabolism
  • Neuromyelitis Optica* / physiopathology
  • Receptors, Interleukin-6 / antagonists & inhibitors*

Substances

  • IL6 protein, human
  • IL6R protein, human
  • Interleukin-6
  • Receptors, Interleukin-6