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Complement activation in patients with neuromyelitis optica

P. Nytrova, E. Potlukova, D. Kemlink, M. Woodhall, D. Horakova, P. Waters, E. Havrdova, D. Zivorova, A. Vincent, M. Trendelenburg,

. 2014 ; 274 (1-2) : 185-91.

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc15007957

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.

Citace poskytuje Crossref.org

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$a Nytrova, Petra $u Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, General University Hospital, Charles University in Prague, Czech Republic; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Electronic address: petranytrova@yahoo.com.
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$a 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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$a Potlukova, Eliska $u Third Department of Medicine, General University Hospital, First Faculty of Medicine, Charles University in Prague, Czech Republic.
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$a Kemlink, David $u Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, General University Hospital, Charles University in Prague, Czech Republic.
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$a Woodhall, Mark $u Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
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$a Horakova, Dana $u Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, General University Hospital, Charles University in Prague, Czech Republic.
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$a Waters, Patrick $u Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
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$a Vincent, Angela $u Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
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