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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Guillain-Barre syndrome serum and anti-Campylobacter antibody do not exacerbate experimental autoimmune neuritis.
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Guillain-Barre syndrome serum and anti-Campylobacter antibody do not exacerbate experimental autoimmune neuritis.

机译：格林-巴利综合征血清和抗弯曲杆菌抗体不会加剧实验性自身免疫性神经炎。

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摘要

To investigate whether antibodies are pathogenic in Guillain-Barre syndrome (GBS), we injected pre-treatment serum from 11 GBS patients intraperitoneally into rats in which the blood-nerve barrier had been opened by induction of mild adoptive transfer experimental autoimmune neuritis. There was no significant clinical, neurophysiological or pathological difference between rats receiving GBS serum compared with those receiving control serum, except that GBS serum caused minor excess weight loss. Murine monoclonal antibody to Campylobacter jejuni and gangliosides also did not exacerbate disease. This experiment failed to show antibody-mediated disease exacerbation and so does not support an antibody-mediated mechanism in GBS.
机译：为了研究抗体是否在格林-巴利综合征（GBS）中具有致病性，我们将11名GBS患者的腹膜内注射预处理血清注入了通过诱导轻度过继转移实验性自身免疫性神经炎而打开血神经屏障的大鼠中。接受GBS血清的大鼠与接受对照血清的大鼠之间没有显着的临床，神经生理或病理学差异，只是GBS血清引起轻微的体重减轻。空肠弯曲杆菌和神经节苷脂的鼠单克隆抗体也没有使疾病恶化。该实验未能显示抗体介导的疾病恶化，因此不支持GBS中的抗体介导机制。

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