Bollensen E, Steck A J, Schachner M
Department of Neurobiology, University of Heidelberg, Federal Republic of Germany.
Neurology. 1988 Aug;38(8):1266-70. doi: 10.1212/wnl.38.8.1266.
The major glycoprotein P0 from human and bovine peripheral nerves carries the L2/HNK-1 and L3 carbohydrate epitopes and is recognized by serum from patients with IgM gammopathy and polyneuropathy. Only serum from patients with reactivity toward the myelin-associated glycoprotein (MAG) was reactive with P0, while serum that did not react with MAG also did not recognize P0. Furthermore, the neural adhesion molecules L1, N-CAM, and J1 were also recognized by the serum that reacted with MAG, while the L3 carbohydrate-carrying cell adhesion molecule AMOG was not recognized. These observations indicate a restricted specificity in carbohydrate reactivity of IgM paraproteins and implicate yet another and, for the first time, peripheral myelin-specific glycoprotein in the pathogenesis of demyelinating neuropathy.
人和牛外周神经中的主要糖蛋白P0携带L2/HNK-1和L3碳水化合物表位,可被IgM丙种球蛋白病和多神经病患者的血清识别。只有对髓鞘相关糖蛋白(MAG)有反应的患者血清才与P0反应,而对MAG无反应的血清也不识别P0。此外,与MAG反应的血清也能识别神经粘附分子L1、N-CAM和J1,而携带L3碳水化合物的细胞粘附分子AMOG则不被识别。这些观察结果表明IgM副蛋白在碳水化合物反应性方面具有受限的特异性,并首次表明另一种外周髓鞘特异性糖蛋白参与了脱髓鞘性神经病的发病机制。