Defining biological subsets in systemic lupus erythematosus: progress toward personalized therapy.
Defining biological subsets in systemic lupus erythematosus: progress toward personalized therapy.
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DOI：
10.1007/s40290-017-0178-6
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发表时间：
2017-04
影响因子：
2.5
通讯作者：
Niewold TB
中科院分区：
文献类型：
--
作者：
Sinicato NA;Postal M;Appenzeller S;Niewold TB
系统性红斑狼疮（SLE）是一种在疾病严重程度、治疗反应和器官损害方面具有异质性的疾病。SLE的发病机制包括遗传和环境因素共同驱动的免疫机制。不同祖先背景的SLE患者在发病机制上存在明显差异，包括遗传危险因素、免疫学参数和临床表现的差异。循环中I型干扰素（IFN）水平高与低的患者代表了SLE中的一个主要生物学亚群，这两组患者存在于所有祖先背景中。遗传因素、自身抗体和其他细胞因子水平在高IFN和低IFN患者之间都不同。这种区别在预测抗I型IFN治疗的反应方面也很重要，为SLE生物学亚群预测治疗反应提供了先例。这篇综述将突出一些最新的发展，在定义生物学亚组的SLE疾病的病理生理学的基础上，和思想，提高知识的疾病异质性将通知我们的努力，个性化治疗这种疾病。
Systemic lupus erythematosus (SLE) is a heterogeneous disease with respect to disease severity, response to treatment, and organ damage. The pathogenesis of SLE includes immunological mechanisms which are driven by both genetic and environmental factors. There are clear differences in the pathogenesis of SLE between patients of different ancestral backgrounds, including differences in genetic risk factors, immunological parameters, and clinical manifestations. Patients with high vs. low levels of type I interferon (IFN) in circulation represents one major biological subset within SLE, and these two groups of patients are present in all ancestral backgrounds. Genetic factors, autoantibodies, and levels of other cytokines all differ between high and low IFN patients. This distinction has also been important in predicting response to treatment with anti-type I IFN therapies, providing a precedent in SLE for biological subsets predicting treatment response. This review will highlight some recent developments in defining biological subsets of SLE based on disease pathophysiology, and the idea that improved knowledge of disease heterogeneity will inform our efforts to personalize therapy in this disease.