Latov N
Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY 10032.
Ann Neurol. 1990;27 Suppl:S41-3. doi: 10.1002/ana.410270711.
Increased titers of IgM antibodies that react with carbohydrate epitopes on GM1 are present in some patients with lower motor neuron disease, sensorimotor neuropathy, or motor neuropathy with or without conduction block. Therapeutic reduction of antibody concentrations can result in clinical improvement, suggesting that the antibodies may be pathogenic. The anti-GM1 antibodies react with carbohydrate epitopes, which are shared by several other glycolipids and glycoproteins in the central and peripheral nervous system. The antibodies might exert their effects at a number of sites, depending on the topographical distribution of the target antigens and on their accessibility. B-cells that express anti-GM1 antibodies are present at birth and are normally suppressed or rendered anergic. Under some circumstances, however, they might be activated to secrete autoantibodies that cause autoimmune neuropathy.
一些患有下运动神经元疾病、感觉运动性神经病变或伴有或不伴有传导阻滞的运动性神经病变的患者体内,与GM1上碳水化合物表位发生反应的IgM抗体滴度升高。抗体浓度的治疗性降低可导致临床症状改善,这表明这些抗体可能具有致病性。抗GM1抗体与碳水化合物表位发生反应,而中枢和周围神经系统中的其他几种糖脂和糖蛋白也具有这些表位。根据靶抗原的拓扑分布及其可及性,这些抗体可能在多个部位发挥作用。表达抗GM1抗体的B细胞在出生时就存在,通常受到抑制或变为无反应性。然而,在某些情况下,它们可能被激活以分泌导致自身免疫性神经病变的自身抗体。