Yamamura Takashi, Ono Hirohiko, Sato Wakiro
Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry.
Brain Nerve. 2018 Jan;70(1):35-40. doi: 10.11477/mf.1416200947.
A recent study on the pathogenesis of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has revealed an elevation of inflammatory and anti-inflammatory cytokines in the sera and cerebrospinal fluids of the patients and presence of autoantibodies in subgroups of ME/CFS patients. Furthermore, investigator-initiated clinical trials have proved the efficacy of anti-CD20 antibody (rituximab), that eliminate B cells, in the treatment of ME/CFS. Based on these findings, we hypothesize that immune abnormalities, such as enhanced autoimmune responses, may play an essential role in the neuroinflammatory pathogenesis of ME/CFS.
最近一项关于肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）发病机制的研究显示，患者血清和脑脊液中的炎性细胞因子和抗炎细胞因子水平升高，且ME/CFS患者亚组中存在自身抗体。此外，研究者发起的临床试验已证明，可消除B细胞的抗CD20抗体（利妥昔单抗）在治疗ME/CFS方面具有疗效。基于这些发现，我们推测免疫异常，如自身免疫反应增强，可能在ME/CFS的神经炎症发病机制中起关键作用。
