Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Front Immunol. 2021 Feb 15;12:625465. doi: 10.3389/fimmu.2021.625465. eCollection 2021.
Here we report three cases of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) mimicking multiple sclerosis in which seropositivity for anti-MOG antibodies occurred during disease-modifying drug dimethyl fumarate (DMF) treatment. These patients developed relapses with anti-MOG antibody seroconversion after switching from fingolimod or steroid pulse therapy to DMF, which was associated with peripheral lymphocyte recovery. MOGAD is considered a humoral immune disease, and DMF reportedly enhances Th2-skewed humoral immune activity. Therefore, we suggest that DMF, but not fingolimod, may exacerbate humoral immune imbalance and enhance autoantibody production, leading to aggravation of MOGAD.
我们在此报告三例抗髓鞘少突胶质细胞糖蛋白(MOG)抗体相关疾病(MOGAD)的病例,这些患者在疾病修正治疗药物富马酸二甲酯(DMF)治疗期间出现抗 MOG 抗体阳性,类似于多发性硬化症。这些患者在从芬戈莫德或类固醇脉冲治疗转换为 DMF 后发生了复发,并伴有抗 MOG 抗体血清转化,这与外周淋巴细胞恢复有关。MOGAD 被认为是一种体液免疫疾病,而 DMF 据报道可增强 Th2 偏倚的体液免疫活性。因此,我们认为 DMF 而非芬戈莫德可能会加剧体液免疫失衡并增强自身抗体的产生,从而导致 MOGAD 加重。