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.

虽然补体依赖性细胞毒性 (CDC) 是水通道蛋白-4-免疫球蛋白 (Ig)G 阳性 (AQP4-IgG+) 视神经脊髓炎谱系障碍 (NMOSD) 的已知效应机制，但 CDC 在髓鞘少突胶质细胞糖蛋白抗体相关疾病中的作用（MOGAD）不太清楚。我们测定了临床稳定的 AQP4-IgG+ NMOSD ( n  = 16)、MOGAD ( n  = 15)、早期多发性硬化症 (MS, n  = 19) 和健康对照 (HC, n  = 18 )患者的补体 C3 和 C4 血浆浓度）。AQP4-IgG+ NMOSD 中的 C4 低于 MOGAD、MS 和 HC（p  < 0.05，成对比较）。AQP4-IgG+ NMOSD 中的 C3 低于 MS（p = 0.034)。这些发现表明在临床稳定的 AQP4-IgG+ NMOSD 中存在细微的补体消耗，但在 MOGAD 中则不然。