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慢性炎症性脱髓鞘性多发性神经根神经病患者循环CD4+CD25+调节性T细胞功能受损。

Impairment of circulating CD4+CD25+ regulatory T cells in patients with chronic inflammatory demyelinating polyradiculoneuropathy.

作者信息

Chi Li-Jun, Wang Hua-Bing, Wang Wei-Zhi

机构信息

Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

出版信息

J Peripher Nerv Syst. 2008 Mar;13(1):54-63. doi: 10.1111/j.1529-8027.2008.00158.x.

Abstract

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated peripheral nervous system disease. CD4+CD25+ T regulatory cells (Tregs) have been unequivocally shown to be critical in maintaining immune tolerance and preventing auto-immune diseases by suppressing self-reactive T cells. Thus, we hypothesized that the numbers and/or the function of Tregs would be deranged during the progressive or relapse phases of CIDP. The number of Tregs was determined by flow cytometry according to their characteristic CD4+CD25(high) membrane phenotype. Functional characterization of Tregs was analyzed by suppression of proliferation and secretion of cytokines by co-cultured effector CD4+CD25- T cells. FOXP3 message expression level was assessed by quantitative real-time polymerase chain reaction. The results showed significant reduction in both the number and the suppressive function of Tregs in the patients with CIDP compared with healthy controls. Also, Tregs isolated from CIDP patients expressed lower levels of FoxP3 mRNA. During the progressive or the relapsing phases of CIDP, the number of Tregs was reduced, and the suppressive function of them decreased. These findings may be helpful to our understanding of the possible role of Tregs in the pathogenesis of CIDP.

摘要

慢性炎性脱髓鞘性多发性神经根神经病(CIDP)是一种免疫介导的周围神经系统疾病。CD4+CD25+调节性T细胞(Tregs)已被明确证明在维持免疫耐受和通过抑制自身反应性T细胞预防自身免疫性疾病方面至关重要。因此,我们推测在CIDP的进展期或复发期,Tregs的数量和/或功能会出现紊乱。根据其特征性的CD4+CD25(高)膜表型,通过流式细胞术测定Tregs的数量。通过共培养效应性CD4+CD25-T细胞对Tregs的增殖抑制和细胞因子分泌进行分析,以对其功能进行表征。通过定量实时聚合酶链反应评估FOXP3信使表达水平。结果显示,与健康对照相比,CIDP患者的Tregs数量及其抑制功能均显著降低。此外,从CIDP患者分离出的Tregs表达的FoxP3 mRNA水平较低。在CIDP的进展期或复发期,Tregs数量减少,其抑制功能下降。这些发现可能有助于我们理解Tregs在CIDP发病机制中的可能作用。

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