Increases in soluble VCAM-1 correlate with a decrease in MRI lesions in multiple sclerosis treated with interferon beta-1b
Increases in soluble VCAM-1 correlate with a decrease in MRI lesions in multiple sclerosis treated with interferon beta-1b
复制标题
DOI：
10.1002/ana.410410517
复制
发表时间：
1997-05-01
影响因子：
11.2
通讯作者：
McFarland, HF
中科院分区：
文献类型：
--
作者：
Calabresi, PA;Tranquill, LR;McFarland, HF
磁共振成像显示，干扰素 β-1b 可减少多发性硬化症的临床恶化和疾病活动，但作用机制尚不清楚。我们研究了干扰素 β-1b 治疗后可溶性粘附分子水平与钆喷酸二葡胺磁共振图像上对比增强病变减少之间的相关性。我们测定了确诊多发性硬化症患者在干扰素 β-1b 治疗前和治疗期间每月血清样本中可溶性血管细胞粘附分子-1、细胞间粘附分子-1、E-选择素、L-选择素和肿瘤坏死因子受体 (60 kd) 的水平。可溶性粘附分子的水平与每月对比增强图像上新增强的病变数量相关。与对照或治疗前的值相比，治疗期间可溶性血管细胞粘附分子的水平显着增加。健康受试者的这种粘附分子的中位水平（ng/ml）为580.3（范围：373.0-640.7），治疗前患者为551.4（489.7-875.5），治疗期间为847.9（591.5-1,232.9）。其他可溶性粘附分子和可溶性肿瘤坏死因子受体的水平在治疗期间没有显着变化。可溶性血管细胞粘附分子的增加与磁共振图像上对比增强病变数量的减少相关。这些数据表明干扰素β-1b通过直接干扰粘附级联而发挥新的作用机制，这可能会阻止活化的T细胞流入中枢神经系统。
Interferon beta-1b reduces clinical exacerbations and disease activity in multiple sclerosis as shown by magnetic resonance imaging, but the mechanism of action is unknown. We investigated the correlation between the levels of soluble adhesion molecules and a reduction in contrast-enhancing lesions on gadopentetate dimeglumine magnetic resonance images after treatment with interferon beta-1b. We determined levels of soluble vascular cell adhesion molecule-1, intercellular adhesion molecule-1, E-selectin, L-selectin, and tumor necrosis factor receptor (60 kd) in monthly serum samples from patients with definite multiple sclerosis before and during treatment with interferon beta-1b. The level of soluble adhesion molecules was correlated with the number of newly enhancing lesions on monthly contrast-enhanced images. Levels of soluble vascular cell adhesion molecule during treatment were significantly increased compared to control or pretreatment values. The median levels (ng/ml) of this adhesion molecule were 580.3 (range; 373.0-640.7) for the healthy subjects, and 551.4 (489.7-875.5) for patients prior to treatment and 847.9 (591.5-1,232.9) during treatment. Levels of the other soluble adhesion molecules and soluble tumor necrosis factor receptor were not significantly changed during treatment. The increase in soluble vascular cell adhesion molecule correlated with a decrease in the number of contrast-enhancing lesions on magnetic resonance images. These data suggest a novel mechanism of action for interferon beta-1b by direct interference with the adhesion cascade, which may prevent activated T cells from trafficking into the central nervous system.