Meléndez-Vásquez C, Redford J, Choudhary P P, Gray I A, Maitland P, Gregson N A, Smith K J, Hughes R A
Department of Neurology, UMDS, Guy's Hospital, London, UK.
J Neuroimmunol. 1997 Mar;73(1-2):124-34. doi: 10.1016/s0165-5728(96)00189-0.
In order to investigate the hypothesis that chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disease related to the acute inflammatory form of Guillain-Barre Syndrome (GBS), we studied 40 patients, 40 age and sex matched controls with other forms of peripheral neuropathy (ONP) and 37 controls from the same family or household (FC). We sought antibodies to gangliosides GM1 and LM1 by enzyme linked immunoassay (ELISA) confirmed by immuno-overlay. Only 6 (15%) CIDP patients had IgM antibodies to ganglioside GM1 (GM1) and none had IgG antibodies. We found IgM antibodies to ganglioside LM1 in 2 (5%) and IgG antibodies in 4 (10%) CIDP patients. Antibodies of IgG or IgM class were detected by ELISA to chondroitin sulphate C or sulfatide in up to 7.5% of CIDP patients. There were IgM antibodies in 3 (7.5%) and IgG in 4 (10%) patients against 25, 28 or 36 kD myelin proteins identified by immunoblot. Antibodies to any of these candidate myelin autoantigens were not significantly more frequent in CIDP than FC or ONP controls. Sera from 5 CIDP patients with active disease which subsequently responded to plasma exchange did not induce more demyelination upon intraneural injection into rat sciatic nerve than ONP sera. Serum tumor necrosis factor alpha (TNFalpha) concentrations were not increased in any of the CIDP patients. Serological evidence of Campylobacter jejuni (Cj) infection was present in 4 (10%) CIDP patients. IgM antibodies to cytomegalovirus (CMV) were not detected in any sera. CIDP is not commonly associated with either of these infections or with an antibody-mediated response to any of these glycolipid or myelin autoantigens.
为了研究慢性炎症性脱髓鞘性多发性神经根神经病（CIDP）是一种与急性炎症形式的吉兰 - 巴雷综合征（GBS）相关的自身免疫性疾病这一假说，我们研究了40例患者、40例年龄和性别匹配的患有其他形式周围神经病（ONP）的对照者以及37例来自同一家族或家庭的对照者（FC）。我们通过酶联免疫吸附测定（ELISA）并经免疫印迹确认来寻找针对神经节苷脂GM1和LM1的抗体。仅有6例（15%）CIDP患者具有针对神经节苷脂GM1（GM1）的IgM抗体，且无人具有IgG抗体。我们在2例（5%）CIDP患者中发现了针对神经节苷脂LM1的IgM抗体，在4例（10%）CIDP患者中发现了IgG抗体。通过ELISA检测到高达7.5%的CIDP患者存在针对硫酸软骨素C或硫脂的IgG或IgM类抗体。3例（7.5%）患者存在针对通过免疫印迹鉴定的25、28或36 kD髓鞘蛋白的IgM抗体，4例（10%）患者存在IgG抗体。CIDP患者中针对这些候选髓鞘自身抗原中任何一种的抗体在频率上并不显著高于FC或ONP对照者。5例患有活动性疾病且随后对血浆置换有反应的CIDP患者的血清在注射到大鼠坐骨神经内时，与ONP血清相比并未诱导出更多的脱髓鞘。任何CIDP患者的血清肿瘤坏死因子α（TNFα）浓度均未升高。4例（10%）CIDP患者存在空肠弯曲菌（Cj）感染的血清学证据。在任何血清中均未检测到针对巨细胞病毒（CMV）的IgM抗体。CIDP通常与这些感染中的任何一种均无关联，也与针对这些糖脂或髓鞘自身抗原的抗体介导反应无关。
