J Clin Invest. 2021 Jul 1;131(13). doi: 10.1172/JCI150382.
Fibromyalgia syndrome (FMS) is a highly prevalent, debilitating disease with heterogeneous symptoms of widespread pain and tenderness, fatigue, sleep disturbance, and impaired cognition. The cause of FMS is unknown, but the clinical constellation of symptoms and abnormalities in the neuroendocrine system, autonomic nervous system, and sleep implicate the nervous system in its pathogenesis. In this issue of the JCI, Goebel, Krock, et al. identified antibodies from patients with FMS that produce FMS in mice by binding to satellite glial cells (SGCs), which envelope sensory neurons. Because antibodies harvested from patients with FMS, but not controls, stimulated SGCs to an activated state known to mediate chronic pain by augmenting neuronal activity, these findings reveal a pivotal role for autoreactive IgG in the pathophysiology of FMS. These important findings pave a pathway to study mechanism-based experimental therapeutics targeting IgG titers or antibody binding to SGCs underlying the neuroimmune dysfunction of FMS.
纤维肌痛综合征（FMS）是一种普遍存在且使人虚弱的疾病，其特征为广泛疼痛和压痛、疲劳、睡眠障碍和认知障碍等多种症状。FMS 的病因尚不清楚，但症状的临床特征以及神经内分泌系统、自主神经系统和睡眠异常提示神经系统在其发病机制中起作用。在本期 JCI 中，Goebel、Krock 等人鉴定了来自 FMS 患者的抗体，这些抗体通过与包裹感觉神经元的卫星胶质细胞（SGC）结合在小鼠中产生 FMS。因为从 FMS 患者而不是对照者中采集的抗体刺激 SGC 进入一种已知通过增强神经元活动来介导慢性疼痛的激活状态，这些发现揭示了自身反应性 IgG 在 FMS 病理生理学中的关键作用。这些重要发现为研究针对 IgG 滴度或抗体与 SGC 结合的基于机制的实验治疗铺平了道路，这些抗体是 FMS 神经免疫功能障碍的基础。
