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Updated: Apr 26, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
Published on: August 21, 2017
Complement activation in patients with neuromyelitis optica
Petra Nytrova1, Eliska Potlukova2, David Kemlink3
1Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, General University Hospital, Charles University in Prague, Czech Republic; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Abstract:
The role of complement has been demonstrated in experimental models of neuromyelitis optica (NMO), however, only few studies have analysed complement components longitudinally in NMO patients. We measured serum or plasma concentrations of anti-C1q antibodies and complement split products C3a and C4a and soluble C5b-9 in patients with NMO, multiple sclerosis and healthy controls. NMO patients had higher levels of C3a and anti-C1q antibodies than healthy controls. C3a levels correlated with disease activity, neurological disability and aquaporin-4 IgG in NMO patients suggesting a role of the alternative pathway of complement in the pathogenesis of NMO and supporting the strategy of therapeutic complement inhibition.
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