Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) associated with the destruction of oligodendrocyte-produced myelin, which results in neuron and oligodendrocyte loss (1, 2). The dysregulated activity of cells of the adaptive immune system, specifically T cells and B cells, plays an important role in MS pathology, particularly during the relapsing–remitting phase of the disease. However, innate immune chronic inflammation driven by CNS-resident cells and recruited monocytes is thought to drive CNS pathology in the progressive phase of MS, an MS phase characterized by the progressive and irreversible accumulation of neurologic disability largely unresponsive to available therapeutic approaches (1, 2).

中文翻译：

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TrbK 控制星形胶质细胞驱动的少突胶质细胞铜中毒 [免疫学和炎症]


多发性硬化症 (MS) 是一种中枢神经系统 (CNS) 炎症性疾病，与少突胶质细胞产生的髓鞘质破坏相关，导致神经元和少突胶质细胞损失 ( 1 , 2 )。适应性免疫系统细胞（特别是 T 细胞和 B 细胞）的失调活性在 MS 病理学中发挥着重要作用，特别是在疾病的复发缓解期。然而，由中枢神经系统驻留细胞和募集的单核细胞驱动的先天免疫慢性炎症被认为在多发性硬化症进展期驱动中枢神经系统病理学，这一多发性硬化症阶段的特点是神经功能障碍的进行性和不可逆转的积累，对现有的治疗方法基本上没有反应（ 1 ， 2 ）。