Abstract：
Lupus nephritis (LN) is a common and serious clinical manifestation of systemic lupus erythematosus. However, the pathogenesis of LN is not fully understood. The currently available treatments do not cure the disease and appear to have a variety of side effects in the long term. The purpose of this study was to search for key molecules involved in the LN immune response through bioinformatics techniques to provide a reference for LN-specific targeted therapy. The GSE112943 dataset was downloaded from the Gene Expression Omnibus database, and 20 of the samples were selected for analysis. In total, 2330 differentially expressed genes were screened. These genes were intersected with a list of immune genes obtained from the IMMPORT immune database to obtain 128 differentially expressed immune-related genes. Enrichment analysis showed that most of these genes were enriched in the interferon signalling pathway. Gene set enrichment analysis revealed that the sample was significantly enriched for expression of the interferon signalling pathway. Further analysis of the core gene cluster showed that nine genes, GBP2, VCAM1, ADAR, IFITM1, BST2, MX2, IRF5, OAS1 and TRIM22, were involved in the interferon signalling pathway. According to our analysis, the guanylate binding protein 2 (GBP2), interferon regulatory factor 5 and 2\'-5\'-oligoadenylate synthetase 1 (OAS1) genes are involved in three interferon signalling pathways. At present, we do not know whether GBP2 is associated with LN. Therefore, this study focused on the relationship between GBP2 and LN pathogenesis. We speculate that GBP2 may play a role in the pathogenesis of LN as a member of the interferon signalling pathway. Further immunohistochemical results showed that the expression of GBP2 was increased in the renal tissues of LN patients compared with the control group, confirming this conjecture. In conclusion, GBP2 is a member of the interferon signalling pathway that may have implications for the pathogenesis of LN and serves as a potential biomarker for LN.
摘要：
狼疮性肾炎(LN)是系统性红斑狼疮常见且严重的临床表现。然而,LN的发病机制尚不完全清楚。目前可用的治疗方法无法治愈该疾病，并且从长远来看似乎具有多种副作用。本研究旨在通过生物信息学技术寻找参与LN免疫应答的关键分子,为LN特异性靶向治疗提供参考。GSE112943数据集从基因表达综合数据库下载，并选择20个样品进行分析。总的来说,筛选了2330个差异表达基因。将这些基因与从IMMPORT免疫数据库获得的免疫基因列表相交,以获得128个差异表达的免疫相关基因。富集分析表明，这些基因中的大多数在干扰素信号通路中富集。基因集富集分析揭示样品显著富集了干扰素信号传导途径的表达。对核心基因簇的进一步分析显示,9个基因,GBP2,VCAM1,ADAR,IFITM1、BST2、MX2、IRF5、OAS1和TRIM22参与干扰素信号通路。根据我们的分析,鸟苷酸结合蛋白2（GBP2），干扰素调节因子5和2'-5'-寡腺苷酸合成酶1（OAS1）基因参与三种干扰素信号通路。目前,我们不知道GBP2是否与LN相关。因此,本研究主要探讨GBP2与LN发病机制的关系。我们推测GBP2可能作为干扰素信号通路的成员在LN的发病机制中起作用。进一步免疫组化结果显示,与对照组相比,LN患者肾组织中GBP2的表达增加,证实了这个猜想。总之,GBP2是干扰素信号通路的成员，可能对LN的发病机理有影响，并作为LN的潜在生物标志物。
