Discoid lupus erythematosus (DLE) is a disorder of the immune system commonly seen in women of childbearing age. The pathophysiology and aetiology are still poorly understood, and no cure is presently available. Therefore, there is an urgent need to explore the underlying molecular mechanisms, as well as search for new therapeutic targets. Gene expression data from skin biopsies samples of DLE patients and healthy controls were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) between DLE and healthy control samples were identified by differential expression analysis. Samples were analysed using CIBERSORT to examine the proportion of immune infiltration. Weighted gene co-expression network analysis was used to screen for the module most relevant to immune infiltration. Candidate genes were uploaded to the TRRUST database to obtain the potential transcription factors regulating these genes. Protein–protein interaction (PPI) analysis was performed to obtain the hub genes most associated with immune infiltration among the candidate genes. A total of 273 DEGs were identified between the DLE and healthy control samples. The results of immunoinfiltration analysis showed that the abundances of resting memory CD4 T cells, activated memory CD4 T cells and M1 macrophages were significantly higher, while those of resting infiltration of plasma cells, regulatory T cells and dendritic cells were lower in DLE samples than in healthy control samples. Correlation analysis showed that ISG15, TRIM22, XAF1, IFIT2, OAS2, OAS3, OAS1, IFI44, IFI6, BST2, IFIT1 and MX2 were negatively correlated with the abundances of plasma cells, T-cell regulatory cells and resting dendritic cells and positively correlated with activated memory CD4 T cells and M1 macrophages. Our study shows that these hub genes may regulate DLE via immune-related pathways mediated by the infiltration of these immune cells.

盘状红斑狼疮 (DLE) 是一种常见于育龄妇女的免疫系统疾病。其病理生理学和病因学仍知之甚少，目前尚无治愈方法。因此，迫切需要探索其潜在的分子机制，并寻找新的治疗靶点。DLE 患者和健康对照的皮肤活检样本的基因表达数据从 Gene Expression Omnibus 数据库下载。通过差异表达分析鉴定了 DLE 和健康对照样本之间的差异表达基因 (DEG)。使用 CIBERSORT 分析样品以检查免疫浸润的比例。使用加权基因共表达网络分析来筛选与免疫浸润最相关的模块。将候选基因上传至TRRUST数据库，以获得调节这些基因的潜在转录因子。进行蛋白质-蛋白质相互作用（PPI）分析，以获得候选基因中与免疫浸润最相关的中心基因。在 DLE 和健康对照样本之间总共鉴定出 273 个 DEG。免疫浸润分析结果显示，DLE样本中静息记忆CD4 T细胞、活化记忆CD4 T细胞和M1巨噬细胞的丰度显着升高，而浆细胞、调节性T细胞和树突状细胞的静息浸润丰度低于DLE样本。健康对照样品。相关分析显示ISG15、TRIM22、XAF1、IFIT2、OAS2、OAS3、OAS1、IFI44、IFI6、BST2、IFIT1 、 MX2与浆细胞、T细胞调节细胞、静息树突状细胞丰度呈负相关，与浆细胞、T细胞调节细胞、静息树突状细胞丰度呈正相关。激活记忆 CD4 T 细胞和 M1 巨噬细胞。我们的研究表明，这些中枢基因可能通过这些免疫细胞浸润介导的免疫相关途径来调节 DLE。