Abstract：Objective: This study aims to investigate the mechanism of EBV infection in T cells by sequencing the transcriptome of EBV-stimulated Jurkat T cells overexpressing CD21. Methods: The target gene CD21 was cloned by PCR and inserted into an overexpression lentiviral vector via molecular cloning techniques, ensuring its stable overexpression on the surface of Jurkat T cells. The CD21-overexpressing Jurkat T cells were then stimulated with EBV(EBV-LV-Jurkat). Transcriptome sequencing was performed on EBV-stimulated CD21-overexpressing Jurkat T cells, untreated Jurkat T cells, and Jurkat T cells infected with lentivirus alone(LV-Jurkat). Gene set enrichment analysis was conducted on differentially expressed genes (DEGs) between EBV-stimulated CD21-overexpressing Jurkat T cells (EBV-LV-Jurkat T) and CD21-overexpressing Jurkat T cells (LV-Jurkat T). Results: GO enrichment analysis of DEGs between EBV-LV-Jurkat T and LV-Jurkat T revealed significant enrichment in the molecular function of MAP kinase tyrosine phosphatase activity , involving the DUSP1, DUSP10, DUSP5, and DUSP8 genes. KEGG pathway enrichment analysis of DEGs indicated that multiple pathways and molecules, similar to those observed in EBV-infected B cells, were significantly enriched in the MAPK, IL-17, HIF-1, NF-κB, and PI3K/AKT signaling pathways, and genes related to the immune response system. Conclusion: This study successfully constructed a model of CD21-overexpressing Jurkat T cells and revealed the impact of EBV stimulation on significantly activating the MAPK signaling pathway, providing crucial preliminary data for further exploration of the mechanism of EBV infection in T cells.
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2024, Vol. 30 
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