Rechtman Ariel, Zveik Omri, Shweiki Lyne, Hoichman Garrick, Friedman-Korn Tal, Brill Livnat, Vaknin-Dembinsky Adi
Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.
Front Immunol. 2025 Jul 24;16:1620069. doi: 10.3389/fimmu.2025.1620069. eCollection 2025.
Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are autoimmune central nervous system disorders with poorly understood immune pathways. CD83 plays a crucial role in the development and maintenance of immune tolerance. This study aims to evaluate CD83 expression in NMOSD and MOGAD and its correlation with disease activity.
RNA extracted from PBMCs of MOGAD, NMOSD and healthy controls (HCs) was analyzed to assess CD83 expression levels. ELISA was used to quantify soluble CD83 (sCD83) levels in the CSF and serum of patients. Additionally, the effects of therapeutic agents used for CNS demyelinating diseases on sCD83 expression levels were examined. The study enrolled 231 untreated participants, including 64 with MOGAD, 56 with NMOSD, 47 with MS, and 64 HCs.
NMOSD patients exhibited lower sCD83 levels compared to MOGAD and HCs, and MOGAD patients with a relapsing course had lower sCD83 levels than those with a monophasic course. Lower sCD83 levels correlated with a severe disease course. Treatment with IVIG and azathioprine significantly increased sCD83 levels in the patients' serum. treatment with immunosuppressives led to a significant increase in sCD83 levels with the most pronounced effect observed following treatment with mycophenolate mofetil.
Our study consistently found lower sCD83 levels in NMOSD and relapsing MOGAD patients. sCD83 levels increased following IVIG and immunosuppressive therapy. This elevation may reflect either a direct effect of the therapy itself, or a compensatory rebound response following immune suppression. These findings highlight the potential of sCD83 as a prognostic biomarker in these diseases and support its role as both a therapeutic target and a marker for treatment response in CNS demyelinating disorders.
视神经脊髓炎谱系障碍（NMOSD）和髓鞘少突胶质细胞糖蛋白抗体相关疾病（MOGAD）是自身免疫性中枢神经系统疾病，其免疫途径尚不清楚。CD83在免疫耐受的发展和维持中起关键作用。本研究旨在评估CD83在NMOSD和MOGAD中的表达及其与疾病活动的相关性。
分析从MOGAD、NMOSD患者及健康对照（HC）的外周血单核细胞（PBMC）中提取的RNA，以评估CD83表达水平。采用酶联免疫吸附测定（ELISA）法对患者脑脊液和血清中的可溶性CD83（sCD83）水平进行定量。此外，还研究了用于中枢神经系统脱髓鞘疾病的治疗药物对sCD83表达水平的影响。该研究纳入了231名未接受治疗的参与者，包括64例MOGAD患者、56例NMOSD患者、47例多发性硬化症（MS）患者和64名HC。
与MOGAD患者和HC相比，NMOSD患者的sCD83水平较低，复发型MOGAD患者的sCD83水平低于单相病程患者。较低的sCD83水平与严重的病程相关。静脉注射免疫球蛋白（IVIG）和硫唑嘌呤治疗可显著提高患者血清中的sCD83水平。免疫抑制剂治疗导致sCD83水平显著升高，其中霉酚酸酯治疗后效果最为明显。
我们的研究始终发现NMOSD患者和复发型MOGAD患者的sCD83水平较低。IVIG和免疫抑制治疗后sCD83水平升高。这种升高可能反映了治疗本身的直接作用，或者是免疫抑制后的代偿性反弹反应。这些发现突出了sCD83作为这些疾病预后生物标志物的潜力，并支持其作为中枢神经系统脱髓鞘疾病治疗靶点和治疗反应标志物的作用。
