The transcriptional profiling identifies hub genes in immune subsets of patients with Behçet's syndrome.

Abstract

Behçet's syndrome (BS) is a variable vessel vasculitis characterised by heterogeneity of organ manifestations. Antigen-presenting cells, such as macrophages and T cells, play critical roles in their immunopathology. This study aimed to identify hub genes and biological processes in patients with BS. We downloaded expression profiles, GSE61399, containing CD14+ monocytes and CD4+T cells between BS and healthy controls from the Gene Expression Omnibus (GEO). We screened the differential expression genes (DEGs) by the GEO2R. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Protein-protein interaction (PPI) network and core genes were analysed by the Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape with Molecular Complex Detection (MCODE) plug-in tools. We identified 102 DEGs in CD14+ monocytes and 48 in CD4+ T cells. In monocytes, the gene enrichment was mainly involved in type I interferon signaling pathway, defense response to virus, cell chemotaxis, granulocyte chemotaxis, granulocyte migration, leukocyte chemotaxis, and neutrophil chemotaxis. The changed genes in CD4+ cells were enriched in MyD88-dependent toll-like receptor signaling pathway, positive regulation of innate immune response, and IL1B production. In combination with PPI and Markov Cluster Algorithm (MCL), we defined three driving protein-protein modules, IL1B, CCL2, CCL4, CXCL2, CCL20, CXCL3, TLR6, CD83, IFIT3, and THBD as a set of hub genes in CD14+ monocytes, associated with inflammation and thrombosis; CD300LF, CLEC5A, DMXL2, MS4A14, TMEM176A in CD4+ T cells. Our findings provide novel insights into the immune subsets related to the biological process in BS, which could contribute to identifying potential biomarkers and novel treatment strategies for BS.