Zhu J, Mix E, Link H
Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
J Neuroimmunol. 1998 Apr 1;84(1):40-52. doi: 10.1016/s0165-5728(97)00238-5.
Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome, GBS) and its animal model experimental autoimmune neuritis (EAN) are prototypes of T cell-mediated autoimmune diseases affecting the peripheral nervous system (PNS). Perivascular accumulation of macrophages and T lymphocytes in the PNS, and high levels systemically of PNS myelin antigen-reactive T cells are characteristic features of both diseases, thereby suggesting a pathogenic role for immunoregulatory cytokines. Here we summarise recent studies that have clearly documented that Th1/Th2/Th3 cytokines are differently upregulated during various clinical phases of EAN and GBS. The observations indicate that the role of cytokines in immune regulation and autoimmune disease is more complex than a simple Th1-Th2 dichotomy would suggest. New treatments may be searched for that counteract this complex cytokine imbalance. Treatments with antibodies that selectively target certain pro-inflammatory cytokines, as well as with immunomodulatory preparations that promote cytokines that beneficially influence the disease course should be in focus of future therapeutic trials.
急性炎性脱髓鞘性多发性神经根神经病（吉兰 - 巴雷综合征，GBS）及其动物模型实验性自身免疫性神经炎（EAN）是影响外周神经系统（PNS）的T细胞介导的自身免疫性疾病的原型。PNS中巨噬细胞和T淋巴细胞的血管周围积聚，以及全身高水平的PNS髓鞘抗原反应性T细胞是这两种疾病的特征性表现，从而提示免疫调节细胞因子具有致病作用。在此，我们总结了最近的研究，这些研究清楚地证明了Th1/Th2/Th3细胞因子在EAN和GBS的不同临床阶段有不同程度的上调。这些观察结果表明细胞因子在免疫调节和自身免疫性疾病中的作用比简单的Th1-Th2二分法所提示的更为复杂。可能需要寻找新的治疗方法来对抗这种复杂 的细胞因子失衡。选择性靶向某些促炎细胞因子的抗体治疗，以及促进对疾病进程有有益影响的细胞因子的免疫调节制剂治疗，应成为未来治疗试验的重点。
