GRN和KLRB1定义了一个共享的外周血液转录组签名,将SLE和IPF联系起来
Lijun Pang1, Yunfei Li1, Junjie Chen1
1Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, 230038, China.
Journal of translational autoimmunity
|March 5, 2026
概括
这项研究确定了外围血液中共享的基因表达模式,将系统性红斑狼 (SLE) 和异常性肺纤维化 (IPF) 联系起来. 这些发现支持对这些免疫炎症疾病的诊断模型的开发.
科学领域:
- 免疫学 免疫学 免疫学
- 基因组学就是基因组学.
- 翻译医学是一种翻译医学.
背景情况:
- 系统性红斑狼 (SLE) 和异常性肺纤维化 (IPF) 具有共同的免疫-炎症特征.
- 连接SLE和IPF的外周血液中精确的转录组签名尚未完全理解.
研究的目的:
- 确定外围血液中共享的基因表达程序,将SLE与IPF联系起来.
- 为这两种疾病优先选择可靠的标记物.
- 开发和验证使用这些标记物的诊断模型.
主要方法:
- 来自SLE和IPF发现和验证队伍的外周血液转录组的分析.
- 利用差异表达分析和加权基因共同表达网络分析 (WGCNA).
- 使用共识特征选择方法 (LASSO,SVM-RFE,随机森林) 和在多个队列和实验环境中验证的模型开发了节的基因组.
主要成果:
- 确定了43个协调调节的共享差异表达基因 (DEG) 和43个共享模块基因,形成了78个B细胞和髓状细胞通路丰富的候选基因池.
- 开发了SLE的6基因小组和IPF的4基因小组,在发现和验证队列中实现了高曲线下面积 (AUC) 值.
- 实验验证证证实SLE患者的基因组失调和血清粒素 (GRN) 升高,与疾病活性标志物相关.
结论:
- 粒素 (GRN) 和KLRB1是连接SLE和IPF的共享外周血液转录基因特征的关键组成部分.
- 开发的诊断模型在多个队列和实验证据中显示出强大的验证.
- 在不同的炎症条件下,模型的性能有所不同,这凸显了对特定上下文的解释和验证的需要.
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