Identification and localization of minor glycolipid antigens recognized by serum antibody in Guillain-Barre' syndrome

由于血浆置换的有效性，包括自身抗体在内的体液因素可能在格林-巴利综合征（GBS）的发病过程中起作用。据报道，在GBS急性期血清中，患者中存在针对几种糖脂的血清抗体，其滴度随着临床改善而降低。由于少数未鉴定的糖脂也可能是GBS血清中抗体的靶点，我们使用薄层色谱（TLC）免疫染色法测定了针对粗神经节苷脂组分的血清抗体。在50例GBS患者中的6例中检测到针对仅在GD 1a以下迁移的条带的抗体活性。通过DEAE-Sephadex A-25柱层析、唾液酸酶处理和Iatrobeads柱层析分离未鉴定的糖脂。快原子轰击质谱表明其为GalNAc-GD 1a。所有6例患者在GBS神经系统发作前均患有胃肠道感染，复合肌肉动作电位振幅较低 关于我们 神经传导速度正常或仅轻微下降。因此，这种抗体可能会提高GBS与轴突损伤或脱髓鞘的变化，在最远端的周围神经。未来的研究是必要的，以确定定位的GalNAc-GD 1a。肺炎支原体（Mycoplasma pneumoniae，MP）是GBS的前驱感染之一，82例GBS患者中有4例在发病前有支原体感染，4例患者均检测到抗半乳糖苷（Gal-C）抗体。78例非支原体感染的GBS患者中2例有抗Gal-C抗体，而所有GBS患者及正常对照组均无抗Gal-C抗体，因此抗Gal-C抗体可能是支原体感染后GBS的特征性升高。Gal-C是髓鞘中的重要抗原，已报道Gal-C致敏可引起兔抗体介导的脱髓鞘性神经病。抗Gal-C抗体可能在支原体感染后GBS患者脱髓鞘性神经病变的病理生理机制中起作用。少

Because of the effectiveness of plasmapheresis, humoral factors including autoantibodies may function in the pathogenetic process of Guillain-Barre' syndrome (GBS). Serum antibodies against several glycolipids have been reported in patients in the acute phase sera of GBS,their titers decreasing with clinical improvement. Because minor unidentified glycolipids also may be targets of antibodies in GBS sera, we assayd serum antibody against a crude ganglioside fraction using thin-layr chromatogram (TLC) immunostaining. Antibody activity was detected against a band that migrated just below GD1a in 6 of the 50 patients with GBS tested. The unidentified glycolipid was isolated by DEAE-Sephadex A-25 column chromatography, sialidase treatment, and Iatrobeads column chromatography. Fast atom bombardment-mass spectra showed it to be GalNAc-GD1a. All 6 patients had suffered gastrointestinal infection before the neurological onset of GBS and showed low amplitudes for the compound muscle action pot … More entials and normal or only slightly decreased nerve conduction velocities. Therefore, this antibody may be raised in GBS with axonal damage or demyelinative change in the most distal sites of the peripheral nerve. Future study is necessary for determining localization of GalNAc-GD1a. Mycoplasma pneumoniae is one agent of the infections preceding GBS.Four of 82 patients with GBS suffered from mycoplasma infection before onset of GBS.All four patients had antibody against galactocerebroside (Gal-C). Two of 78 patients with GBS without mycoplasma infection had anti-Gal-C antibody but none of the disease or normal controls had it. Thus anti-Gal-C antibody may be characteristically raised in GBS subsequent to mycoplasma infection. Gal-C is known to be an important antigen in myelin, and sensitization to Gal-C has been reported to cause antibody-mediated demyelinative neuropathy in rabbit. The anti-Gal-C antibodies may function in the pathophysiologic mechanism of demyelinative neuropathy in patients with GBS subsequent to mycoplasma infection. Less