Caudie C, Vial C, Bancel J, Petiot P, Antoine J C, Gonnaud P M
Service d'immunologie et de neuro-immunologie, Hôpital neurologique et neurochirurgical, 69394 Lyon cedex 03.
Ann Biol Clin (Paris). 2002 Sep-Oct;60(5):589-97.
We established anti-ganglioside antibody profiles in GBS and studied the frequency, fine specificity and clinical correlate. IgG and IgM antibodies to 8 gangliosides were tested by immunodot-blot in 249 consecutive patients with Guillain-Barré syndrome with large variability in clinical expression, referred to our laboratory over a 8-year period. IgG and IgM anti-GM1 antibodies were measured by Elisa. Thin-layer chromatography overlayed by serum was used to control positivity. 89/249 GBS (36%) had characteristic anti-ganglioside antibody profile. Isotypes were, IgG (62%), IgG + IgM (26%) and IgM (12%). Antecedent infections were found in 62% of GBS included more frequently Campylobacter jejuni and cytomegalovirus. Various autoantibody profiles were described with an immunodominant ganglioside. We detected 6 characteristic anti-ganglioside profiles with fine specificity and immunodominant ganglioside corresponding to 6 immuno-clinical variants of GBS: 1) anti-GM1 and GD1b IgG and IgG > IgM in the acute motor axonal neuropathy after Campylobacter jejuni infection in 41 GBS; 2) anti-GD1a IgG in 6 severe motor axonal GBS after Campylobacter jejuni infection; 3) selectively anti-GQ1b IgG in 17 typical Miller Fisher syndrome with areflexia, ataxia and ophthalmoplegia; 4) anti- GT1b ganglioside and polysialogangliosides IgG (n = 9) in two separate cranial nerve variants, ophthalmoplegic SGB and lower cranial nerve variants depending upon the presenting deficit; 5) anti-GD1b IgG in 5 pure ataxic sensory GBS (4%); 6) anti-GM2 IgM in 11 severe GBS with antecedent CMV infection (8%). 34 GBS (14%) had low levels of anti-GM1 and GD1b IgM antibodies which are not disease specific and may simply represent part of the naturally occurring autoantibody population or a secondary response to disease. 126 GBS (50%) had no antibodies, predominantly in classical form. Associations between isotype, fine specificity and clinical presentation permit the definition of homogeneous immuno-clinical variants. Various autoantibody profiles with diagnostic and prognostic value are easy to perform by immunodot blot in acute peripheral neuropathies.
我们建立了吉兰 - 巴雷综合征（GBS）的抗神经节苷脂抗体谱，并研究了其频率、精细特异性及临床相关性。在8年期间，我们实验室共接收了249例临床表现差异较大的连续性吉兰 - 巴雷综合征患者，通过免疫斑点印迹法检测了针对8种神经节苷脂的IgG和IgM抗体。采用酶联免疫吸附测定法检测IgG和IgM抗GM1抗体。利用血清覆盖的薄层色谱法控制阳性结果。249例GBS患者中有89例（36%）具有特征性的抗神经节苷脂抗体谱。其亚型分别为：IgG（62%）、IgG + IgM（26%）和IgM（12%）。62%的GBS患者有前驱感染史，其中空肠弯曲菌和巨细胞病毒感染更为常见。我们描述了多种具有免疫显性神经节苷脂的自身抗体谱。我们检测到6种具有精细特异性且免疫显性神经节苷脂对应的特征性抗神经节苷脂谱，分别对应GBS的6种免疫临床变异型：1）41例空肠弯曲菌感染后急性运动轴索性神经病患者中，抗GM1和GD1b IgG且IgG > IgM；2）6例空肠弯曲菌感染后严重运动轴索性GBS患者中，抗GD1a IgG；3）17例典型的伴有无反射、共济失调和眼肌麻痹的米勒 - 费希尔综合征患者中，选择性抗GQ1b IgG；4）在两种不同的颅神经变异型中，即眼肌麻痹性SGB和低位颅神经变异型（取决于所表现的缺陷），抗GT1b神经节苷脂和多唾液酸神经节苷脂IgG（n = 9）；5）5例纯共济失调性感觉GBS（4%）中，抗GD1b IgG；6）11例有巨细胞病毒前驱感染的严重GBS患者中，抗GM2 IgM（8%）。34例GBS（14%）抗GM1和GD1b IgM抗体水平较低，这些抗体并非疾病特异性的，可能仅代表自然存在的自身抗体群体的一部分或对疾病的继发性反应。126例GBS（50%）无抗体，主要为经典型。抗体亚型、精细特异性与临床表现之间的关联有助于定义同质的免疫临床变异型。在急性周围神经病中，通过免疫斑点印迹法可轻松检测到具有诊断和预后价值的多种自身抗体谱。
