Mäurer M, Toyka K V, Gold R
Department of Neurology, Clinical Research Group for Multiple Sclerosis and Neuroimmunology, Julius-Maximilians-Universität Würzburg, Germany.
Rev Neurol (Paris). 2002 Dec;158(12 Pt 2):S7-15.
Autoimmune demyelinating neuropathies, like Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), are characterized by local inflammation and demyelination of peripheral nerves. The therapeutic response to plasma exchange and IVIg points to an important role for humoral factors in the pathogenesis of these autoimmune disorders of the peripheral nervous system (PNS). The similarity of the human disease with its animal model disease experimental autoimmune neuritis (EAN), and the activation of T-cell and macrophage derived cytokines all indicate that cellular immunity is also of relevance. Many of the basic principles in autoimmune inflammatory neuropathies have been learned from studies in EAN which can now be linked to the human disorders. This article summarizes current aspects of cellular immunity in autoimmune demyelinating disorders of the PNS. Better understanding of these cellular immunoregulatory mechanisms may help to develop new therapeutic strategies.
自身免疫性脱髓鞘性神经病，如吉兰 - 巴雷综合征（GBS）和慢性炎症性脱髓鞘性多发性神经病（CIDP），其特征是周围神经的局部炎症和脱髓鞘。对血浆置换和静脉注射免疫球蛋白的治疗反应表明体液因素在这些周围神经系统（PNS）自身免疫性疾病的发病机制中起重要作用。人类疾病与其动物模型疾病实验性自身免疫性神经炎（EAN）的相似性，以及T细胞和巨噬细胞衍生细胞因子的激活均表明细胞免疫也与之相关。自身免疫性炎性神经病的许多基本原理已从EAN的研究中得知，现在这些原理可与人类疾病联系起来。本文总结了PNS自身免疫性脱髓鞘疾病中细胞免疫的当前研究情况。更好地理解这些细胞免疫调节机制可能有助于开发新的治疗策略。
