目的：本研究旨在根据2017年McDonald标准分析早期RRMS中T调节性T（Treg）细胞产生的促炎和抗炎细胞因子的血清和脑脊液（CSF）浓度。
目的：多发性硬化症（MS）是一种慢性，炎症，中枢神经系统（CNS）的脱髓鞘疾病，细胞因子网络起着重要作用。然而,关于早期RRMS的免疫发病机制的数据一直缺乏，特别是根据2017年麦当劳标准。
方法：研究组包括复发期间的早期RRMS患者（n=18），缓解（n=14），和对照组。MS诊断是根据2017年麦当劳标准建立的。在做出诊断后1年内对患者进行研究。基于ELISA的定量测试试剂盒用于血清和CSF中的细胞因子测量。TNF-α水平的比较和相关性分析，TGF-β2，IgG指数，并进行复发持续时间。
结果：与对照组相比，在RRMS复发和RRMS缓解组中，TNF-α的CSF浓度均显着升高（p<0.01）。与对照组相比，RRMS复发组的TGF-β2的CSF水平显着降低（p=0.01）。
结论：在早期RRMS中似乎发生了不适当的炎症反应，包括TNF-α的产生和TGF-β2释放的减少，这表明Treg细胞具有重要作用。对该主题的进一步研究可能有助于开发新的疾病改善药物和该疾病的生化标志物。
OBJECTIVE: This study aimed to analyze serum and cerebrospinal fluid (CSF) concentrations of proinflammatory and anti-inflammatory cytokines produced by T regulatory (Treg) cells in early RRMS according to the 2017 McDonald criteria.
OBJECTIVE: Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS) with the cytokine network playing an important role. However, there is a continual lack of data regarding the immunopathogenesis of early RRMS, especially according to the 2017 McDonald criteria.
METHODS: The study groups included early RRMS patients during relapse (n = 18), remission (n = 14), and the control group. The MS diagnosis was established according to the 2017 McDonald criteria. Patients were studied up to 1 year after diagnosis was made. A quantitative test kit based on ELISA was used for cytokine measurement in the serum and CSF. Comparative and correlation analyses between the levels of TNF-α, TGF-β2, IgG index, and relapse duration were performed.
RESULTS: Significantly higher CSF concentrations of TNF-α in both RRMS-relapse and RRMS-remission groups were found compared to the controls (p < 0.01). The CSF levels of TGF-β2 in the RRMS-relapse group were significantly lower in comparison to the control group (p = 0.01).
CONCLUSIONS: An inappropriate inflammatory response seems to occur in early RRMS and includes the production of TNF-α and a decrease in TGF-β2 release suggesting a significant Treg cells role. Further studies on the topic may contribute to developing new disease-modifying drugs and biochemical markers of the disorder.
