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格林-巴利综合征患者的 T 细胞在受到神经节苷脂 GM1 刺激时会产生干扰素-γ。

T cells from patients with Guillain-Barré syndrome produce interferon-gamma in response to stimulation with the ganglioside GM1.

机构信息

Centre for Clinical Research, The Royal Brisbane and Women's Hospital, The University of Queensland, Herston Road, Herston, Queensland 4029, Australia.

出版信息

J Clin Neurosci. 2010 Apr;17(4):537-8. doi: 10.1016/j.jocn.2009.07.096. Epub 2010 Jan 25.

Abstract

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.

摘要

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。

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