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

Identification and localization of minor glycolipid antigens recognized by serum antibody in Guillain-Barre' syndrome
格林-巴利综合征血清抗体识别的次要糖脂抗原的鉴定和定位
批准号:
05670551
负责人:
KUSUNOKI Susumu
金额:
$1.34万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1993
资助国家:
日本
项目状态:
已结题
起止时间:
1993 至 1994

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中文摘要
翻译
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)的发病过程中发挥作用。已有报道在GBS急性期患者中发现了几种糖脂抗体,其滴度随着临床的改善而下降。由于少量未识别的糖脂也可能是GBS血清中抗体的目标,我们使用薄层色谱(TLC)免疫染色分析了针对粗神经节苷脂部分的血清抗体。在检测的50例GBS患者中,有6例检测到针对GD1a以下的条带的抗体活性。用DEAE-Sephadex A-25柱层析、唾液酸酶处理和医用珠柱层析分离未鉴定的糖脂。快原子轰击-质谱图表明它是GalNAc-GD1a。所有6名患者在神经性GBS发作之前都有胃肠道感染,复合肌肉动作POT…波幅低。神经传导速度正常或仅有轻微减慢。因此,这种抗体可能在周围神经最远端轴突受损或脱髓鞘改变的GBS中升高。进一步的研究对于确定GalNAc-GD1a的定位是必要的。肺炎支原体是GBS前感染的病原体之一,82例GBS患者中有4例在GBS发病前已有支原体感染,4例均有抗半乳糖脑苷类抗体(Gal-C)。78例无支原体感染的GBS患者中有2例抗Gal-C抗体阳性,而GBS患者和正常对照组均未检出Gal-C抗体。因此,在支原体感染后的GBS中可能会出现特异性的抗Gal-C抗体升高。Gal-C是髓鞘中的一种重要抗原,已有报道称对Gal-C的增敏可导致抗体介导的脱髓鞘神经病。抗Gal-C抗体可能在GBS患者支原体感染后脱髓鞘神经病的病理生理机制中发挥作用。较少
英文摘要
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
期刊论文(48)
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会议论文
Kusunoki S,et al.: "Localization of GM1 and GD1b antigens in the human peripheral nervous system." Muscle & Nerve. 16. 752-756 (1993)
Kusunoki S 等人:“GM1 和 GD1b 抗原在人类周围神经系统中的定位”。
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通讯作者:
Arasaki K,et al.: "Acute conduction block in vitro following exposure to antiganglioside sera." Muscle & Nerve. 16. 587-593 (1993)
Arasaki K 等人:“暴露于抗神经节苷脂血清后体外急性传导阻滞。”
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通讯作者:
Kusunoki S, et al.: "Localization of GM1 and GD1b antigents in the human peripheral nervous system" Muscle & Nerve. 16. 752-756 (1993)
Kusunoki S 等人:“GM1 和 GD1b 抗原在人类周围神经系统中的定位”肌肉
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Nishiyama K,et al: "Carcinomatous neuropathy associated with hepatic cell carcinoma:an autopsy case report" Neuromuscular Disorders. 3. 227-229 (1993)
Nishiyama K 等人:“与肝细胞癌相关的癌性神经病:尸检病例报告”神经肌肉疾病。
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