Centre for Clinical Research, The Royal Brisbane and Women's Hospital, The University of Queensland, Herston Road, Herston, Queensland 4029, Australia.
J Clin Neurosci. 2010 Apr;17(4):537-8. doi: 10.1016/j.jocn.2009.07.096. Epub 2010 Jan 25.
Guillain-Barré syndrome (GBS) is an acquired demyelinating neuropathy, characterized by infiltration of peripheral nerves with macrophages and T cells. There have been reports of antibodies to glycolipids in GBS. We have previously found T cell reactivity to glycolipids in patients with the demyelinating form of GBS. This study was performed to characterize the cytokines produced by these T cells. Peripheral blood lymphocytes from patients with GBS, chronic inflammatory demyelinating polyradiculoneuropathy, healthy control patients and other neuropathies were incubated with the ganglioside GM1 and transferred to enzyme-linked immunospot plates. The average number per well of spot-forming cells (SFC) in the absence of antigen was counted. The average spontaneous SFC number was subtracted from the average SFC number in the presence of GM1, to produce a corrected SFC. There was significantly increased production of interferon-gamma but not interleukin-5 in response to stimulation with the ganglioside GM1. This could indicate that SFC have a role in pathogenesis of disease.
格林-巴利综合征(GBS)是一种获得性脱髓鞘神经病,其特征是外周神经被巨噬细胞和 T 细胞浸润。已有报道称 GBS 患者存在针对神经节苷脂的抗体。我们之前发现 GBS 脱髓鞘型患者的 T 细胞对神经节苷脂有反应性。本研究旨在对这些 T 细胞产生的细胞因子进行特征描述。将 GBS 患者、慢性炎症性脱髓鞘性多发性神经病、健康对照患者和其他神经病患者的外周血淋巴细胞与神经节苷脂 GM1 孵育,并转移到酶联免疫斑点平板上。在没有抗原的情况下,每孔斑点形成细胞(SFC)的平均数量被计数。从 GM1 存在时的平均 SFC 数量中减去平均自发 SFC 数量,以产生校正的 SFC。与 GM1 刺激相比,干扰素-γ的产生显著增加,但白细胞介素-5 没有增加。这可能表明 SFC 在疾病发病机制中起作用。