Cytokines and adhesion molecules in multiple sclerosis patients treated with interferon-β1b
Cytokines and adhesion molecules in multiple sclerosis patients treated with interferon-β1b
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DOI：
10.1016/j.cyto.2004.09.005
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发表时间：
2005-01-07
期刊：
影响因子：
3.8
通讯作者：
Sellebjerg, F
中科院分区：
文献类型：
--
作者：
Jensen, J;Krakauer, M;Sellebjerg, F
多发性硬化症 (MS) 是一种中枢神经系统 (CNS) 炎症性脱髓鞘疾病，被认为是由 T 细胞介导的对 CNS 髓磷脂和轴突的攻击引起的。重组干扰素 (IFN)-β 是多发性硬化症的一种既定治疗方法，已知可以减少疾病复发的次数以及不可逆转的疾病症状和体征的发展。然而，IFN-β 治疗的作用机制尚不完全清楚。先前的研究表明对单核细胞细胞因子产生和 T 细胞迁移有重大影响，但结果不一致。我们发现，在接受 IFN-β1b 从头治疗的多发性硬化症患者中，CD49d/VLA-4 分子的 CD4 和 CD8 T 细胞表达降低，可溶性血管细胞粘附分子 (sVCAM-1) 血浆浓度增加，肿瘤坏死因子和白细胞介素 (IL)-12 p40 链血浆浓度增加。我们发现 IFN-β1b 治疗引起的不同变化之间只有微小的关联。我们的研究结果与 T 细胞 CD49d/VLA-4 表达的变化和 sVCAM-1 的诱导一致，这是 IFN-β1b 治疗多发性硬化症的重要作用，而 TNF 和 IL-12 p40 链浓度变化的作用更难以解释。 (C) 2004 Elsevier Ltd. 保留所有权利。
Multiple sclerosis (MS), an inflammatory, demyelinating disease of the central nervous system (CNS), is thought to be caused by a T cell-mediated attack on CNS myelin and axons. Recombinant interferon (IFN)-beta is an established treatment of multiple sclerosis, and is known to reduce the number of disease relapses and the development of irreversible symptoms and signs of disease. The mechanism of action of IFN-beta treatment is, however, not completely understood. Previous studies have suggested major effects on mononuclear cell cytokine production and T cell migration, but results have been inconsistent. We found decreases in CD4 and CD8 T cell expression of the CD49d/VLA-4 molecule, increases in plasma concentrations of soluble vascular cell adhesion molecule (sVCAM-1), and increases in plasma concentrations of tumor necrosis factor and interleukin (IL)-12 p40 chain in patients with MS who were initiated on de novo treatment with IFN-beta1b. We found only minor associations between the different changes induced by IFN-beta1b-treatment. Our findings are consistent with changes in T cell expression of CD49d/VLA-4 and induction of sVCAM-1 as important effects of treatment with IFN-beta1b in multiple sclerosis, whereas the role of changes in TNF and IL-12 p40 chain concentrations is more difficult to interpret. (C) 2004 Elsevier Ltd. All rights reserved.