| Literature DB >> 34464830 |
Florence Pache1, Marius Ringelstein2, Orhan Aktas3, Ingo Kleiter4, Sven Jarius5, Nadja Siebert6, Judith Bellmann-Strobl6, Friedemann Paul7, Klemens Ruprecht8.
Abstract
While complement-dependent cytotoxicity (CDC) is a known effector mechanism in aquaporin-4-immunoglobulin (Ig)G-positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD), the role of CDC in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is less clear. We determined complement C3 and C4 plasma concentrations in patients with clinically stable AQP4-IgG+ NMOSD (n = 16), MOGAD (n = 15), early multiple sclerosis (MS, n = 19) and in healthy controls (HC, n = 18). C4 was lower in AQP4-IgG+ NMOSD than in MOGAD, MS and HC (p < 0.05, pairwise comparisons). C3 was lower in AQP4-IgG+ NMOSD than in MS (p = 0.034). These findings suggest subtle complement consumption in clinically stable AQP4-IgG+ NMOSD, but not in MOGAD.Entities:
Keywords: Antibodies; Aquaporin-4; C3; C4; Complement; Myelin oligodendrocyte glycoprotein; Neuromyelitis optica spectrum disorder
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Year: 2021 PMID: 34464830 DOI: 10.1016/j.jneuroim.2021.577699
Source DB: PubMed Journal: J Neuroimmunol ISSN: 0165-5728 Impact factor: 3.478