1. The role of T cells and shared genes in psoriasis and inflammatory bowel disease based on single-cell RNA and comprehensive analysis.
- Author
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Liang, Xiaofeng, Peng, Zhishen, Deng, Ying, Lin, Xiaobing, Chen, Runnan, Niu, Yujing, Lin, Weiyi, Lin, Zien, Lai, Kuan, and Wei, Shanshan
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INFLAMMATORY bowel diseases , *RNA analysis , *T cells , *GENE expression , *T cell receptors , *GENES , *PSORIASIS - Abstract
• We identified aberrantly activated and differentiated CD4+ and γδ T cells as the immunological mechanisms both in psoriasis and IBD, and IL17 and TNF signaling as the common pathogenesis. • We also found that hub shared genes, LCN2, CXCL1 and PI3, which are involved in psoriasis and IBD, are potential therapeutic targets. Psoriasis and inflammatory bowel disease (IBD) have a similar etiology, including abnormal activation of T cells. Differentially expressed genes (DEGs) analysis was used to search for shared genes. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis were then performed. Secondly, single-cell RNA analysis (scRNA-seq) and immune infiltration were employed to explore the immune imbalance of the diseases. By weighted gene co expression network analysis (WGCNA), we obtained hub shared genes. Furthermore, we analyzed the diagnostic performance and immune association with the hub genes. Finally, functional enrichment of miRNAs related to hub shared genes was carried out. Single-cell analysis showed a high proportion of T cells among infiltrated immune cells and immune infiltration showed CD4+ T and γδ T cells were significantly elevated in diseases. Hub shared genes, LCN2, CXCL1 and PI3 had excellent diagnostic properties and were positively correlated with neutrophils, CD4+ T and γδ T cells. IL17 and TNF signaling pathway were the common pathway. In conclusion, CD4+ and γδ T cells and hub shared genes may play a crucial part in common mechanism between psoriasis and IBD. Moreover, hub shared genes may be potential diagnostic markers. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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