Although T helper 17 (Th17) lymphocytes protect mucosal barriers against infections, they have been implicated in the development of multiple sclerosis (MS). RORC and DDX5 can regulate Th17 differentiation and the development of MS. Since RMRP, as a long non-coding RNA (lncRNA), can mediate the RORC-DDX5 complex, this lncRNA can be involved in developing MS. This study investigated the expression levels of RORC, DDX5, and RMRP in treatment-naïve relapsing-remitting multiple sclerosis (RRMS) patients, healthy controls, and RRMS patients treated with IFNβ-1α or fingolimod, or dimethyl fumarate (DMF), or glatiramer acetate (GA). There was substantial up-regulation in the expression of RORC, DDX5, and RMRP in treatment-naïve RRMS patients compared to healthy controls. Among the comparisons of their expressions in the different groups of treated patients with treatment-naïve patients, only the down-regulation of the RMRP expression level was significant in IFNβ-1α-treated patients. Also, these changes were more pronounced in female patient groups. Our analyses have highlighted the high diagnostic value of RORC, DDX5, and RMRP in treatment-naïve RRMS patients. Furthermore, RMRP has demonstrated moderate positive correlations with the expression of DDX5 and RORC in treated RRMS patients.

尽管T辅助17（Th17）淋巴细胞保护粘膜屏障免受感染，但它们与多发性硬化症（MS）的发生有关。RORC和DDX5可以调节Th17分化和MS的发展。由于RMRP作为长的非编码RNA（lncRNA），可以介导RORC-DDX5复合体，因此该lncRNA可能参与了MS的发展。这项研究调查了未治疗的复发缓解型多发性硬化症（RRMS）患者，健康对照组以及接受IFNβ-1α或芬戈莫德，富马酸二甲酯（DMF）或格拉替雷治疗的RRMS患者中RORC，DDX5和RMRP的表达水平醋酸盐（GA）。与健康对照组相比，未接受过治疗的RRMS患者中RORC，DDX5和RMRP的表达明显上调。在不同治疗组和未治疗患者之间的表达比较中，只有IFNβ-1α治疗的患者中RMRP表达水平的下调是显着的。而且，这些变化在女性患者组中更为明显。我们的分析突出了RORC，DDX5和RMRP在未接受过治疗的RRMS患者中的诊断价值。此外，在治疗的RRMS患者中，RMRP已证明与DDX5和RORC的表达呈中等正相关。