Commentary 10.1172/JCI138804

Microglia complement astrocytes in neuromyelitis optica

Zahra Moinfar and Scott S. Zamvil

Department of Neurology, Weill Institute of Neurosciences and Program in Immunology, UCSF, San Francisco, California, USA.

Address correspondence to: Scott S. Zamvil, Department of Neurology, UCSF, 675 Nelson Rising Lane, NS-215A, San Francisco, California 94158, USA. Phone: 650.799.2101; Email: zamvil@ucsf.neuroimmunol.org.

Find articles by Moinfar, Z. in: JCI | PubMed | Google Scholar

Department of Neurology, Weill Institute of Neurosciences and Program in Immunology, UCSF, San Francisco, California, USA.

Address correspondence to: Scott S. Zamvil, Department of Neurology, UCSF, 675 Nelson Rising Lane, NS-215A, San Francisco, California 94158, USA. Phone: 650.799.2101; Email: zamvil@ucsf.neuroimmunol.org.

Find articles by Zamvil, S. in: JCI | PubMed | Google Scholar

First published June 22, 2020 - More info

J Clin Invest. https://doi.org/10.1172/JCI138804.
© 2020 American Society for Clinical Investigation
First published June 22, 2020 - Version history

Neuromyelitis optica (NMO) is a central nervous system (CNS) inflammatory autoimmune disease caused by antibodies against aquaporin-4 (AQP4) expressed on astrocytes. Binding of AQP4-specific antibodies (NMO-IgG) triggers activation of the complement cascade, which is responsible for astrocyte loss and secondary demyelination. Although the role for the cytolytic complement proteins in astrocyte destruction in NMO is well established, little is known regarding the initial phase of astrocyte injury. In this issue of the JCI, Chen and colleagues evaluated the precytolytic phase when NMO-IgG binds astrocytes in vivo in the absence of exogenous complement. NMO-IgG alone caused astrocyte activation and AQP4 loss. Surprisingly, microglia, CNS-resident innate immune cells that produce endogenous complement, were required for clinical manifestations of disease, a finding that suggests microglia may serve as a therapeutic target in NMO.

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