Willison H J, Trapp B D, Bacher J D, Dalakas M C, Griffin J W, Quarles R H
National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Muscle Nerve. 1988 Nov;11(11):1169-76. doi: 10.1002/mus.880111111.
IgM monoclonal antibodies present in the sera from some patients with peripheral neuropathy react with an antigenic carbohydrate determinant that is present on the myelin-associated glycoprotein (MAG) and other peripheral nerve glycoproteins and glycolipids. It is generally believed that the neuropathy in these patients may be caused by antibody- mediated nerve damage. Intraneural injection of serum from patients with this disease produced an extensive inflammatory, macrophage-mediated demyelination of feline peripheral nerve. This only occurred with very fresh sera which had been supplemented with additional complement. Injection of sera from normal subjects failed to produce any demyelination. These results are in accordance with a recent study by Hays et al. and contradict earlier negative reports of similar studies. It is important to note that the pathology observed in these experimental studies bears little resemblance to that seen in the human neuropathy, and caution must therefore be exercised when interpreting this data in relation to the pathogenic mechanisms that might operate in the human disease.
一些患有周围神经病的患者血清中存在的IgM单克隆抗体与一种抗原性碳水化合物决定簇发生反应,该决定簇存在于髓鞘相关糖蛋白(MAG)以及其他周围神经糖蛋白和糖脂上。一般认为,这些患者的神经病可能是由抗体介导的神经损伤所致。向猫的周围神经进行神经内注射患有这种疾病患者的血清,会产生广泛的、由巨噬细胞介导的猫周围神经脱髓鞘。这仅在补充了额外补体的非常新鲜的血清中才会发生。注射正常受试者的血清未能产生任何脱髓鞘现象。这些结果与海斯等人最近的一项研究一致,并且与早期类似研究的阴性报告相矛盾。需要注意的是,在这些实验研究中观察到的病理学与人类神经病中所见的情况几乎没有相似之处,因此在解释这些数据与可能在人类疾病中起作用的致病机制的关系时必须谨慎。