[Monoclonal IgM autoantibody activity vis-à-vis glycoconjugates of peripheral nerves: apropos of 112 cases].
[Monoclonal IgM autoantibody activity vis-à-vis glycoconjugates of peripheral nerves: apropos of 112 cases].
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[单克隆 IgM 自身抗体相对于周围神经糖缀合物的活性：112 例]。
DOI：
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发表时间：
2001
影响因子：
0.5
通讯作者：
P. Gonnaud
中科院分区：
文献类型：
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作者：
C. Caudie;C. Vial;P. Petiot;J. Bancel;C. Lombard;P. Gonnaud
用不同的免疫学方法测定了112例与单克隆IgM（M-IgM）有关的神经病患者血清中抗糖脂和糖蛋白糖表位的IgM和IgG自身抗体。用间接免疫荧光显微镜检测M-IgM抗髓鞘抗体，用Western印迹法检测M-IgM抗髓鞘相关糖蛋白（MAG）抗体，用薄层层析法检测M-IgM抗SGPG和SGLPG抗体，用膜免疫斑点印迹法检测M-IgM抗神经节苷脂GM 3、GM 2、GD 3、GM 1、GD 1a、GD 1b、GT 1b、GQ 1b和抗硫脂抗体。在112份M-IgM中，有81份（72%）对集中在周围神经的神经糖脂抗原有自身抗体活性。M-IgM在34.5%的病例中与髓鞘强结合，在38%的病例中与MAG强结合，在52%的病例中与SGPG/SGLPG强结合，在21.5%的病例中与神经节苷脂强结合，在26%的病例中与硫苷脂强结合。已经描述了与不同临床综合征相关的六种M-IgM自身抗体活性谱：-在慢性脱髓鞘敏感性和感觉运动性周围神经病中针对糖脂SGPG和SGLPG以及髓鞘相关糖蛋白（MAG）共有的碳水化合物表位的M-IgM自身抗体活性谱（58例患者，52%）; -脱髓鞘纯运动神经病中针对免疫显性GM 1的M-IgM自身抗体活性谱（9例患者，8%）; -慢性脱髓鞘敏感性共济失调性神经病中针对免疫显性二唾液酸神经节苷脂的M-IgM自身抗体活性谱（8例患者，7%）; -脱髓鞘运动性多发性神经病中针对免疫显性GM 2的M-IgM自身抗体活性特征（3例患者，2.5%）; -纯运动性多发性神经病中针对免疫显性GD 1a的M-IgM自身抗体活性特征（2例患者，2%）; -1例急性多发性神经根神经病（1%）中针对免疫显性GT 1b和多唾液酸神经节苷脂的M-IgM自身抗体活性特征。M-IgM可识别除GM 1和GM 2外的所有神经节苷脂。与自身反应特异性IgM单克隆丙种球蛋白病相关的神经病形成不同的综合征。在27.5%的病例中，M-IgM没有可识别的活性自身抗体。
Serum IgM and IgG autoantibodies against carbohydrate epitopes on glycolipids and glycoproteins have been determined in a series of 112 neuropathies associated with monoclonal IgM (M-IgM) by different immunological techniques. The M-IgM anti-myelin sheath antibodies were determined by indirect immunofluorescence microscopy, the M-IgM anti-myelin associated glycoprotein (MAG) antibodies by western-blot analysis, the M-IgM anti-SGPG and SGLPG antibodies by immunodetection on thin-layer chromatography, the M-IgM anti-ganglioside GM3, GM2, GD3, GM1, GD1a, GD1b, GT1b, GQ1b and anti-sulfatide antibodies by immunodot-blot assay on membrane. Among the 112 M-IgM, 81 had autoantibody activity against nerve glycolipid antigens concentrated in peripheral nerve (72%). M-IgM bound strongly to myelin sheath in 34,5% of cases, to MAG in 38% of cases, to SGPG/SGLPG in 52% of cases, to gangliosides in 21.5% of cases and to sulfatide in 26 % of cases. Six M-IgM autoantibody activity profiles have been described in correlation with distinct clinical syndromes: - the M-IgM autoantibody activity profile against the carbohydrate epitope common to the glycolipids SGPG and SGLPG and myelin associated glycoprotein (MAG) in chronic demyelinating sensitive and sensorimotor peripheral neuropathies (58 patients, 52%); - the M-IgM autoantibody activity profile against immunodominant GM1 in demyelinating pure motor neuropathies (9 patients, 8%); - the M-IgM autoantibody activity profile against immunodominant disialosylgangliosides in chronic demyelinating sensitive ataxic neuropathies (8 patients, 7%); - the M-IgM autoantibody activity profile against immunodominant GM2 in demyelinating motor polyneuropathies (3 patients, 2.5%); - the M-IgM autoantibody activity profile against immunodominant GD1a in pure motor polyneuropathies (2 patients, 2%); - the M-IgM autoantibody activity profile against immunodominant GT1b and polysialosylgangliosides in one acute polyradiculoneuropathy (1%). The M-IgM recognized all gangliosides except GM1 and GM2. The neuropathies associated with IgM monoclonal gammopathy with autoreactive specificity form distinct syndromes. In 27.5% of cases, M-IgM had no identifiable activity autoantibodies.