Interferon-β exacerbates Th17-mediated inflammatory disease.
Interferon-β exacerbates Th17-mediated inflammatory disease.
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DOI：
10.1016/j.it.2011.03.008
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发表时间：
2011-06
影响因子：
16.8
通讯作者：
Steinman L
中科院分区：
文献类型：
--
作者：
Axtell RC;Raman C;Steinman L
干扰素-β (IFN-β)是复发缓解型多发性硬化症（RRMS）最常用的治疗药物。然而，30-50%的MS患者对IFN-β没有反应。在某些情况下，IFN-β加重多发性硬化症，并持续加重视神经脊髓炎（NMO）。为了避免对IFN-β无反应的患者进行不必要的治疗，并避免可能的伤害，研究人员正在确定在治疗开始前预测结果的生物标志物。这些生物标志物揭示了对疾病机制的见解。最近在RRMS、NMO、牛皮癣、类风湿关节炎、系统性红斑狼疮和溃疡性结肠炎患者的人体样本中发现，当Th17免疫反应突出时，IFN-β是无效的，并可能使多种疾病的临床状况恶化。
Interferon-β (IFN-β) is the treatment most often prescribed for relapsing-remitting multiple sclerosis (RRMS). However, 30–50% of MS patients do not respond to IFN-β. In some cases, IFN-β exacerbates MS, and it consistently worsens neuromyelitis optica (NMO). In order to eliminate unnecessary treatment for patients non-responsive to IFN-β, and to avoid possible harm, researchers are identifying biomarkers that predict outcome prior to the initiation of treatment. These biomarkers reveal insights into mechanisms of disease. Recent discoveries on human samples from patients with RRMS, NMO, psoriasis, rheumatoid arthritis, systemic lupus erythematosus and ulcerative colitis, indicate that IFN-β is ineffective and may worsen the clinical status in diverse diseases when a Th17 immune response is prominent.