The regulatory effect of IRF8 on the gene expression profiles of bone marrow derived dendritic cells

To investigate the role of IRF8 in the inflammatory microenvironment of abdominal aortic aneurysm tissue, bone marrow cells were isolated from the tibias and femurs of 8-week-old male mice and cultured with granulocyte-macrophage colony-stimulating factor and Flt3L cytokines to generate CD103-positive dendritic cells. Cells were harvested on days 9 and 15-16 and stimulated with tumor necrosis factor-alpha. Gene ontology analysis revealed upregulation of T cell activation and chemotaxis in bone marrow-derived dendritic cells from IRF8 overexpression mice, indicating IRF8's role in dendritic cell-T cell interactions. Protein-protein interaction analysis highlighted Cd40 and Fcgr1 as key surface markers. IRF8-related genes were enriched in type I interferon signaling pathways, implicating IRF8 in antigen presentation functions of dendritic cells. 8-week-old male mice, both wild-type and genetically modified IRF8 overexpression mice were be used. Bone marrow were extracted from the tibias and femurs, and the cells were cultured in RPMI 1640 medium supplemented with granulocyte-macrophage colony-stimulating factor (GM-CSF) and Flt3L cytokines to generate CD103-positive dendritic cells. On days 9 and 15-16, non-adherent dendritic cells were harvested and stimulated with tumor necrosis factor-alpha. Comparisons of gene expression profiles and enrichment differences were conducted between Irf8-OE mice and control ones