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[免疫介导性神经病中的体液抗体]

[Humoral antibodies in immune mediated neuropathy].

作者信息

Saito T

机构信息

Department of Neurology, Kitasato University East Hospital.

出版信息

Rinsho Shinkeigaku. 1990 Dec;30(12):1364-7.

PMID:1966017
Abstract

Immune mediated neuropathy includes acute inflammatory demyelinating polyneuropathy (AIDP), chronic inflammatory demyelinating neuropathy (CIDN), paraproteinemic polyneuropathy (PPN) and Crow-Fukase syndrome (CFS). Serum antibodies as humoral immunity in patients with immune mediated neuropathy were measured by the method of immunoblots and ELISA. P0 protein, P2 protein, 170K-Mr glycoprotein and ganglioside (GGD) of human peripheral nerve myelin and MBP, myelin associated glycoprotein (MAG) of human central nerve myelin were used as antigens. In AIDP anti P2 antibodies were elevated significantly. However, anti MBP antibodies were also elevated in parallel. In PPN anti MAG antibodies were detected in 4 patients with IgM-M proteinemia and demyelinating neuropathy. High titers of anti MAG antibodies were also detected in the same 4 patients. Characteristic pathological findings of biopsied sural nerve were segmental demyelination with widening of the intraperiod line of the outer myelin lamella in all 4 patients. Positive rate of anti myelin antibodies were 23% in 23 cases with PPN. Anti 170K-Mr glycoprotein was detected only in one patient with IgM-M proteinemia, polyneuropathy and incurable dermatitis. Anti GGD antibodies were not detected in PPN or CFS. A few patients with GBS or CIDN have anti GGD antibodies in ELISA. It is well known that various antibodies to peripheral nerve myelin are detected in neuropathy, especially demyelinating state. The most important antigen established in this study in the pathogenesis of neuropathy is MAG. IgM monoclonal protein including anti MAG antibodies was absorbed by purified MAG completely. Anti 170K Mr glycoprotein was also absorbed by purified 170K-Mr glycoprotein. Role of humoral antibody to peripheral nerve myelin specific 170K-Mr glycoprotein remains to be solved.

摘要

免疫介导性神经病包括急性炎症性脱髓鞘性多发性神经病(AIDP)、慢性炎症性脱髓鞘性神经病(CIDN)、副蛋白血症性多发性神经病(PPN)和克劳-富卡塞综合征(CFS)。采用免疫印迹法和酶联免疫吸附测定法检测免疫介导性神经病患者作为体液免疫的血清抗体。将人周围神经髓鞘的P0蛋白、P2蛋白、170K-Mr糖蛋白和神经节苷脂(GGD)以及人中枢神经髓鞘的髓鞘碱性蛋白(MBP)、髓鞘相关糖蛋白(MAG)用作抗原。在AIDP中,抗P2抗体显著升高。然而,抗MBP抗体也同时升高。在PPN中,4例IgM-M蛋白血症和脱髓鞘性神经病患者检测到抗MAG抗体。在这4例相同患者中也检测到高滴度的抗MAG抗体。所有4例患者腓肠神经活检的特征性病理表现为节段性脱髓鞘,外髓鞘板层内周期线增宽。23例PPN患者中抗髓鞘抗体阳性率为23%。仅在1例IgM-M蛋白血症、多发性神经病和难治性皮炎患者中检测到抗170K-Mr糖蛋白。在PPN或CFS中未检测到抗GGD抗体。少数格林-巴利综合征(GBS)或CIDN患者在酶联免疫吸附测定中有抗GGD抗体。众所周知,在神经病,尤其是脱髓鞘状态下可检测到各种针对周围神经髓鞘的抗体。本研究在神经病发病机制中确立的最重要抗原是MAG。包括抗MAG抗体在内的IgM单克隆蛋白被纯化的MAG完全吸收。抗170K Mr糖蛋白也被纯化的170K-Mr糖蛋白吸收。针对周围神经髓鞘特异性170K-Mr糖蛋白的体液抗体的作用仍有待解决。

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