Abstract

BackgroundSystemic lupus erythematosus (SLE) is a multisystemic, chronic inflammatory disease characterized by destructive systemic organ involvement, which could cause the decreased functional capacity, increased morbidity and mortality. Previous studies show that SLE is characterized by autoimmune, inflammatory processes, and tissue destruction. Some seriously-ill patients could develop into lupus nephritis. However, the cause and underlying molecular events of SLE needs to be further resolved.MethodsThe expression profiles of GSE144390, GSE4588, GSE50772 and GSE81622 were downloaded from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs) between SLE and healthy samples. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments of DEGs were performed by metascape etc. online analyses. The protein–protein interaction (PPI) networks of the DEGs were constructed by GENEMANIA software. We performed Gene Set Enrichment Analysis (GSEA) to further understand the functions of the hub gene, Weighted gene co‐expression network analysis (WGCNA) would be utilized to build a gene co‐expression network, and the most significant module and hub genes was identified. CIBERSORT tools have facilitated the analysis of immune cell infiltration patterns of diseases. The receiver operating characteristic (ROC) analyses were conducted to explore the value of DEGs for SLE diagnosis.ResultsIn total, 6 DEGs (IFI27, IFI44, IFI44L, IFI6, EPSTI1 and OAS1) were screened, Biological functions analysis identified key related pathways, gene modules and co‐expression networks in SLE. IFI27 may be closely correlated with the occurrence of SLE. We found that an increased infiltration of moncytes, while NK cells resting infiltrated less may be related to the occurrence of SLE.ConclusionIFI27 may be closely related pathogenesis of SLE, and represents a new candidate molecular marker of the occurrence and progression of SLE. Moreover immune cell infiltration plays important role in the progession of SLE.

Highlights

  • Systemic lupus erythematosus (SLE) is a multisystemic, chronic inflammatory disease characterized by destructive systemic organ involvement, which could cause the decreased functional capacity, increased morbidity and mortality

  • Wang et al [11] showed that there was the association of abnormal elevations in Interferon Induced Protein With Tetratricopeptide Repeats 3 (IFIT3) with overactive cyclic Guanine monophosphate (GMP)-Adenosine monophosphate (AMP) synthase/Stimulator of interferon genes signaling in human systemic lupus erythematosus monocytes

  • gene ontology (GO) enrichment analysis was used to evaluate the potential mechanism of differentially expressed genes (DEGs) from molecular function, biological process, and cellular component categories

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Summary

Introduction

Systemic lupus erythematosus (SLE) is a multisystemic, chronic inflammatory disease characterized by destructive systemic organ involvement, which could cause the decreased functional capacity, increased morbidity and mortality. Previous studies show that SLE is characterized by autoimmune, inflammatory processes, and tissue destruction. Numerous studies [6,7,8] have demonstrated that the pathophysiological process for the development of SLE are closely associated with the mutation and abnormal expression of genes, which include TNFSF4, NCF1-339, CXorf, etc. A previous study demonstrated that IFI44L promoter methylation as a blood biomarker for systemic lupus erythematosus [9]. Wang et al [11] showed that there was the association of abnormal elevations in IFIT3 with overactive cyclic GMP-AMP synthase/Stimulator of interferon genes signaling in human systemic lupus erythematosus monocytes. It is imperative to explore the accurate molecular targets included in occurrence and progression of SLE, in order to make a contribution to the diagnosis and treatment of SLE

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