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多发性硬化症患者鞘内可溶性CD137释放增加。

Heightened intrathecal release of soluble CD137 in patients with multiple sclerosis.

作者信息

Sharief M K

机构信息

Department of Neuroimmunology, Guy's, King's and St Thomas' School of Medicine, Guy's Hospital, London, UK.

出版信息

Eur J Neurol. 2002 Jan;9(1):49-54. doi: 10.1046/j.1468-1331.2002.00323.x.

Abstract

Human CD137 (ILA/4-1BB), a member of the tumour necrosis factor (TNF) receptor family, regulates the activation and proliferation of immune cells, and may induce apoptosis (programmed cell death) of activated lymphocytes. A soluble form of CD137 (sCD137) released by activated lymphocytes may interfere with the activities of the membrane-bound CD137. This study reports the detection of significantly high intrathecal and systemic levels of sCD137 in patients with clinically active multiple sclerosis (MS) when compared with corresponding levels from patients with clinically stable MS or those with inflammatory and non-inflammatory neurological disorders, or from healthy individuals. Intrathecal concentrations of sCD137 in patients with active MS correlate with the intrathecal release of the soluble death receptor protein Fas, but not with the release of interleukin-2, TNF or the synthesis of immunoglobulins G and M. Results presented here suggest that heightened release of sCD137 is a feature of clinically active MS.

摘要

人类CD137(ILA/4-1BB)是肿瘤坏死因子(TNF)受体家族的一员,可调节免疫细胞的激活和增殖,并可能诱导活化淋巴细胞的凋亡(程序性细胞死亡)。活化淋巴细胞释放的可溶性CD137(sCD137)可能会干扰膜结合型CD137的活性。本研究报告称,与临床病情稳定的多发性硬化症(MS)患者、患有炎症性和非炎症性神经系统疾病的患者或健康个体相比,临床活动期MS患者鞘内和全身sCD137水平显著升高。活动期MS患者鞘内sCD137浓度与可溶性死亡受体蛋白Fas的鞘内释放相关,但与白细胞介素-2、TNF的释放或免疫球蛋白G和M的合成无关。此处呈现的结果表明,sCD137释放增加是临床活动期MS的一个特征。

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