Expression profiling identifies responder and non-responder phenotypes to interferon-β in multiple sclerosis
Expression profiling identifies responder and non-responder phenotypes to interferon-β in multiple sclerosis
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DOI：
10.1093/brain/awg147
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发表时间：
2003-06-01
期刊：
影响因子：
14.5
通讯作者：
McFarland, HF
中科院分区：
文献类型：
--
作者：
Stürzebecher, S;Wandinger, KP;McFarland, HF
自身免疫性疾病，如多发性硬化症的特点是复杂的遗传性状和病理机制，转化为临床异质性。多发性硬化症的这种广泛异质性以及对免疫调节药物的不同生物学反应预计将导致不同的治疗反应。剖析个体患者的治疗反应和生物学特征之间关系的策略不仅作为临床工具有价值，而且有助于更好地了解疾病。在这里，我们解决了在体外和离体RNA表达谱下的一个批准的治疗多发性硬化症，干扰素-β（IFN-β，Betaseron），通过cDNA微阵列，并证明无反应者和响应者表型IFN-β作为评估纵向钆增强MRI扫描和临床疾病活动不同，在他们的离体基因表达谱。这些发现将有助于更好地阐明IFN-β与不同疾病模式相关的作用机制，并最终导致优化治疗。
Autoimmune diseases such as multiple sclerosis are characterized by complex genetic traits and pathomechanisms that translate into clinical heterogeneity. This wide heterogeneity of multiple sclerosis as well as different biological responses to immunomodulatory drugs can be expected to contribute to differential treatment responses. Strategies that dissect the relationship between the treatment response and the biological characteristics in individual patients are valuable not only as a clinical tool, but also in leading to a better understanding of the disease. Here we address the in vitro and ex vivo RNA expression profile under one approved therapy of multiple sclerosis, interferon-beta (IFN-beta, Betaseron), by cDNA microarrays and demonstrate that non-responder and responder phenotypes to IFN-beta as assessed by longitudinal gadolinium-enhanced MRI scans and clinical disease activity differ in their ex vivo gene expression profile. These findings will help to better elucidate the mechanism of action of IFN-beta in relation to different disease patterns and eventually lead to optimized therapy.