Increased B cell activating factor (BAFF) expression in patients with neuromyelitis optica spectrum disorder (NMOSD) is associated with B cell overstimulation, but the underlying mechanism remains unclear. This study aimed to reveal the emerging mechanisms that regulate BAFF expression in the inflammatory process of NMOSD. The results showed that the expression of miR-30b-5p was significantly decreased in NMOSD CD14+ monocytes compared with the normal control. Furthermore, we confirmed that metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) is an upstream target of miR-30b-5p, and it could act as a ceRNA and absorb miR-30b-5p with reduced expression of miR-30b-5p. The low expression of miR-30b-5p could not bind to BAFF messenger RNA (mRNA), which resulted in the overexpression of both BAFF mRNA and protein expression. Overexpression of BAFF could bind to the corresponding receptors on B cells, which may initiate activation and proliferation of B cells and increase their production of autoantibodies. Therefore, these findings interpreted that excessive MALAT1 expression in NMOSD mononuclear macrophages led to increased BAFF expression by targeting miR-30b-5p, which caused B cell autoimmune reaction and autoantibodies production, aggravated the disease progression of NMOSD.

中文翻译：

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过多的 MALAT1 通过上调 BAFF 表达来促进视神经脊髓炎谱系疾病的免疫过程。

视神经脊髓炎谱系障碍 (NMOSD) 患者中 B 细胞激活因子 (BAFF) 表达增加与 B 细胞过度刺激有关，但其潜在机制仍不清楚。本研究旨在揭示 NMOSD 炎症过程中调节 BAFF 表达的新兴机制。结果显示，与正常对照相比，NMOSD CD14+单核细胞中miR-30b-5p的表达显着降低。此外，我们证实转移相关肺腺癌转录1（MALAT1）是miR-30b-5p的上游靶标，它可以作为ceRNA并吸收miR-30b-5p，同时降低miR-30b-5p的表达。miR-30b-5p的低表达不能与BAFF信使RNA（mRNA）结合，导致BAFF mRNA和蛋白表达均过度表达。BAFF的过度表达可以与B细胞上相应的受体结合，从而启动B细胞的激活和增殖并增加其自身抗体的产生。因此，这些研究结果解释了NMOSD单核巨噬细胞中MALAT1过度表达，通过靶向miR-30b-5p导致BAFF表达增加，从而引起B细胞自身免疫反应和自身抗体产生，加剧NMOSD的病情进展。