Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system. The inflammatory and neurodegenerative pathways driving MS are modulated by DNA, lysine, and arginine methylation, as evidenced by studies made possible by novel tools for methylation detection or loss of function. We present evidence that MS is associated with genetic variants and metabolic changes that impact on methylation. Further, we comprehensively review current understanding of how methylation can impact on central nervous system (CNS) resilience and neuroregenerative potential, as well as inflammatory versus regulatory T helper (Th) cell balance. These findings are discussed in the context of therapeutic relevance for MS, with broad implications in other neurologic and immune-mediated diseases.

多发性硬化症（MS）是中枢神经系统的一种慢性炎症性疾病。驱动MS的炎症和神经退行性途径受DNA，赖氨酸和精氨酸甲基化的调节，这一点已通过新型甲基化检测或功能丧失工具的研究得以证明。我们提供的证据表明，MS与影响甲基化的遗传变异和代谢变化有关。此外，我们全面回顾了当前对甲基化如何影响中枢神经系统（CNS）弹性和神经再生潜能以及炎症与调节性T辅助（Th）细胞平衡的理解。这些发现是在MS的治疗相关性的背景下讨论的，在其他神经系统疾病和免疫介导的疾病中具有广泛的意义。