抗NMDAR脑炎中B细胞相关免疫病理机制与治疗进展

B Cell Associated Immunopathological Mechanisms in Anti-NMDAR Encephalitis and Therapeutic Advances

抗N-甲基-D-天冬氨酸受体(NMDAR)脑炎是自身免疫性脑炎中最常见的类型之一,其发病机制与B细胞介导的体液免疫反应产生的抗NMDAR抗体有关。抗NMDAR脑炎患者B细胞表面受体互补决定区3存在特异性核酸排列顺序。CXC趋化因子配体13、白细胞介素-6、白细胞介素-17在B细胞迁移和浸润过程中起重要作用。目前,临床已开始使用利妥昔单抗和托珠单抗治疗抗NMDAR脑炎。未来,深入研究抗NMDAR脑炎中B细胞成熟和克隆分化的分子机制,有助于寻找抗NMDAR脑炎的生物标志物,为疾病的早期诊断和靶向治疗提供理论支持。

Anti-N-methyl-D-aspartate receptor(NMDAR)encephalitis is one of the most common types of autoimmune encephalitis and its pathogenesis is associated with anti-NMDAR antibodies generated by the humoral immune response mediated by B cells.Specific nucleic acid sequence exists in B cell surface receptor complementarity determination region 3 in anti-NMDAR encephalitis patients.The chemokine(C-X-C motif)ligand 13,interleukin-6 and interleukin-17 play important roles in B cell migration and infiltration.At present,rituximab and tolizumab are used clinically to treat anti-NMDAR encephalitis.In the future,in-depth studies on the molecular mechanisms of B cell maturation and clonal differentiation in anti-NMDAR encephalitis will help to find biomarkers for anti-NMDAR encephalitis and provide theoretical support for the early diagnosis and targeted therapy.