Abstract: The essence of tissue repair is a highly coordinated multisystem biological process, with the orderly reconstruction of the vascular network being one of its critical components. Previous research has focused on the regulation of endothelial cells by innate immune cells to promote vascular regeneration. In recent years, researchers have discovered that adaptive immune cells play an important role in regulating tissue repair. However, interactions between adaptive immune cells and vascular endothelial cells remain understudied. Among these, regulatory T cells (Tregs) serve as key functional executors in hypoxic microenvironments. Deepening our understanding of their interactions may clarify how the adaptive immune system regulates vascular reconstruction during tissue repair. This study established a hypoxia model to simulate the hypoxic microenvironment following injury. It upregulated HIF-1α expression in Jurkat T cells and promoted FOXP3 expression in Jurkat T cells, resulting in a Treg phenotype. Co-culture with endothelial cells significantly enhanced endothelial cell migration and tubule formation capabilities. Transcriptome sequencing subsequently revealed that hypoxia-induced primary Treg cells remodeled endothelial function by activating signaling pathways such as VEGF. These findings further elucidate the potential mechanisms by which Treg cells regulate endothelial cells, providing novel therapeutic targets for immune-vascular synergistic therapies.