Tumor necrosis factor (TNF)-like ligand 1A (TL1A) is a member of the TNF family of cytokines, also known as TNFSF15. It is primarily expressed by endothelial cells. In T cells, TL1A acts as a co-stimulatory agent, increasing IL-2 responsiveness and secretion of pro-inflammatory cytokines both in vitro and in vivo. TL1A is the sole known ligand for its receptor “death receptor 3” (DR3, also known as TNFRSF25). DR3 is a tumor necrosis factor family receptor that contains a death domain, highly homologous to TNFR1, upregulated during T cell activation, and induces cell apoptosis. The interaction between DR3 and TL1A can be achieved by blocking the binding of TL1A and DR3. Therefore, TL1A/DR3 can serve as an important potential therapeutic target for chronic immune diseases. Additionally, studies have shown that DR3 agonistic antibodies can reduce the suppressive activity of regulatory T cells and enhance the effector function of CD4+ T cells in a melanoma model in mice, making DR3 agonists potential drugs for treating solid tumors.The Mouse_TNFRSF25(DR3) Reporter Jurkat Cell Line is a luciferase reporter gene cell line with two main applications: first, by adding DR3 agonistic drugs, the downstream signaling pathway of the reporter gene cells can be activated, and luciferase expression can be determined by measuring the fluorescence signal. This can be used for screening or validating DR3-targeting agonistic drugs. Second, by adding TL1A antagonistic antibodies, the downstream signaling of DR3 activated by TL1A-expressing cells can be blocked, and luciferase expression can be determined by measuring the fluorescence signal. This can be used for screening or validating TL1A-targeting antagonistic drugs.
