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首页> 外文期刊>Archives of Neurology >Down-regulation of survivin expression in T lymphocytes after interferon beta-1a treatment in patients with multiple sclerosis.
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Down-regulation of survivin expression in T lymphocytes after interferon beta-1a treatment in patients with multiple sclerosis.

机译：生存素表达的下调T淋巴细胞干扰素beta-1a治疗后多发性硬化症患者。

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BACKGROUND: Treatment with interferon beta reduces clinical exacerbations in multiple sclerosis (MS) through several immunomodulatory mechanisms that involve the augmentation of programmed cell death (apoptosis) of peripheral T lymphocytes. The expression of survivin, a cell cycle-regulated antiapoptosis protein, is up-regulated in mitogen-stimulated T lymphocytes from patients with MS, and this expression correlates with MS disease activity. OBJECTIVE: To evaluate the effect of interferon beta on the expression of survivin and other apoptosis regulatory molecules in peripheral T lymphocytes from patients with MS. PATIENTS AND METHODS: In a prospective, combined clinical and immunologic study, we evaluated the expression of survivin, Bcl-2 protein, and the death receptor Fas in mitogen-stimulated T lymphocytes from 26 patients with MS, before and serially after treatment with interferon beta-1a. We also investigated the long-term effects of interferon beta-1a on cellular expression of these proteins and T-lymphocyte apoptosis in a cross-sectional study of 19 patients with MS receiving long-term interferon beta-1a therapy. RESULTS: Treatment with interferon beta-1a reduced the expression of survivin in in vitro stimulated T lymphocytes. This reduced expression correlated with augmented T-cell susceptibility to apoptosis and with clinical response to treatment. In contrast, interferon beta-1a therapy did not significantly alter cellular expression of Bcl-2 protein or Fas. This down-regulatory effect of interferon beta-1a on cellular expression of survivin was maintained after long-term therapy. CONCLUSIONS: Our observations suggest that interferon beta exerts a regulatory effect on peripheral T lymphocytes through an antiapoptosis mechanism that involves the down-regulation of cellular survivin expression.
机译：背景:治疗干扰素β减少多发性硬化(MS)的临床发作通过几种免疫调节机制包括程序性细胞死亡的增加(凋亡)的外周T淋巴细胞。生存素的表达细胞cycle-regulatedantiapoptosis蛋白质,是上调的mitogen-stimulated从患者T淋巴细胞女士,这个表达式与MS疾病活动。干扰素β表达的效果生存素和其他细胞凋亡调控分子在外围从患者T淋巴细胞病人和方法:女士。她们在一次前瞻性结合临床及免疫学研究中,我们评估生存素的表达,bcl - 2蛋白质,和死亡受体Fasmitogen-stimulated从26患者T淋巴细胞女士,之前和连续治疗后干扰素beta-1a。干扰素beta-1a的长期影响这些蛋白质和细胞的表达早期凋亡的横断面研究19患者接受长期女士干扰素beta-1a疗法。与干扰素beta-1a减少的表达生存素在体外刺激T淋巴细胞。这减少了表达和增强有关t细胞凋亡和易感性临床对治疗的反应。干扰素beta-1a疗法并不显著改变细胞bcl - 2蛋白的表达Fas。beta-1a细胞存活素的表达保持长期治疗后。我们的观察表明,β干扰素施加监管影响周边T淋巴细胞通过一个antiapoptosis机制涉及到细胞的下调生存素的表达。

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