利用基因表达数据对系统性红斑狼疮患者进行分层以揭示不同免疫途径的表达
Stratification of Systemic Lupus Erythematosus Patients Using Gene Expression Data to Reveal Expression of Distinct Immune Pathways
摘要：
系统性红斑狼疮（SLE）是美国15-24岁女性的第十大死亡原因。SLE患者表现出的症状和免疫途径的多样性给治疗SLE以及新的临床试验带来了困难。这项研究使用无监督学习对成年SLE患者的基因表达数据进行分类。基因表达数据的维度通过三种单独的方法（PCA、UMAP和简单的线性自动编码器）降低，并且来自这些方法中的每一种的结果用于将患者用k均值聚类分成六个聚类。这些聚类揭示了SLE患者中导致SLE的三种独立的免疫途径。这些途径是：（1）高干扰素水平，（2）高自身抗体水平，（3）线粒体凋亡途径失调。前两种途径在SLE中已被广泛研究。然而，线粒体凋亡尚未被调查之前，以我们所知，作为一个独立的原因SLE，独立于自身抗体的产生，表明线粒体蛋白可能会导致一组新的治疗靶点SLE在未来的研究。
英文摘要：
Systemic lupus erythematosus (SLE) is the tenth leading cause of death in females 15-24 years old in the US. The diversity of symptoms and immune pathways expressed in SLE patients causes difficulties in treating SLE as well as in new clinical trials. This study used unsupervised learning on gene expression data from adult SLE patients to separate patients into clusters. The dimensionality of the gene expression data was reduced by three separate methods (PCA, UMAP, and a simple linear autoencoder) and the results from each of these methods were used to separate patients into six clusters with k-means clustering. The clusters revealed three separate immune pathways in the SLE patients that caused SLE. These pathways were: (1) high interferon levels, (2) high autoantibody levels, and (3) dysregulation of the mitochondrial apoptosis pathway. The first two pathways have been extensively studied in SLE. However, mitochondrial apoptosis has not been investigated before to the best of our knowledge as a standalone cause of SLE, independent of autoantibody production, indicating that mitochondrial proteins could lead to a new set of therapeutic targets for SLE in future research.
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