Human TNFSF15 (Tumor Necrosis Factor Superfamily Member 15, also known as TL1A or VEGI—vascular endothelial growth inhibitor) is a cytokine belonging to the tumor necrosis factor (TNF) superfamily, which includes related ligands such as TNF-α, Fas ligand (FasL), CD40 ligand (CD40L), TRAIL, and RANKL that regulate immune signaling, apoptosis, and inflammatory processes. In humans, TNFSF15 is primarily produced by endothelial cells, macrophages, dendritic cells, and other immune cells in response to inflammatory stimuli, infection, or tissue injury. TNFSF15 exerts its biological effects mainly through binding to death receptor 3 (DR3, TNFRSF25) expressed on T lymphocytes, particularly Th1 and Th17 cells, activating intracellular signaling pathways including NF-κB and MAPK, which promote T cell activation, cytokine production, and inflammatory responses. In addition to its immune regulatory role, TNFSF15 also influences angiogenesis and vascular homeostasis, where it can inhibit endothelial cell proliferation and contribute to regulation of blood vessel formation. Dysregulation of TNFSF15 signaling has been implicated in several chronic inflammatory and autoimmune diseases, including inflammatory bowel disease (Crohn’s disease and ulcerative colitis), rheumatoid arthritis, and other immune-mediated disorders. Because TNFSF15 is an important regulator of T cell–mediated immunity and vascular biology, it is widely studied in immunology, inflammation research, and therapeutic development targeting TNF superfamily signaling pathways.