{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTNFRSF25—commonly known as death receptor 3 (DR3)—functions as a key immunomodulatory receptor whose engagement by its ligand TL1A orchestrates diverse inflammatory responses. In the immune compartment, DR3 is expressed on multiple lymphocyte subsets including memory CD4⁺ T cells, innate lymphoid cells, and natural killer cells. Its activation enhances T helper 2 effector responses that drive allergic lung inflammation, promotes Th17 differentiation in rheumatoid arthritis, and bolsters innate cytokine output from group 3 innate lymphoid cells, while simultaneously expanding regulatory T cells that temper overt immune activation. Aberrant DR3 expression is also observed in inflammatory conditions such as psoriasis, preeclampsia, kidney transplant rejection, and in barrier tissues where cells coexpress DR3 together with IL‑18 receptors, thereby contributing to antigen‐independent innate responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its immunoregulatory roles, DR3 signaling critically governs cell fate by dictating pro-survival versus death responses. In hematopoietic and cancer cell models, engagement of DR3 by TL1A induces the assembly of a receptor complex that triggers NF‑κB activation and upregulation of anti‑apoptotic proteins; yet under certain conditions, DR3 signaling also promotes caspase‐dependent apoptosis and, intriguingly, can induce necroptosis via RIP1/RIP3 pathways. These cell death mechanisms have been linked to modulation of cancer cell migration and survival in colon and breast carcinomas, with altered DR3 expression or even gene duplication events being associated with autoimmune susceptibility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐documented immunological and apoptotic roles, TNFRSF25 signaling exerts significant functions in non‑immune tissues that influence tissue remodeling and homeostasis. In the bone microenvironment, DR3 activity modulates osteoclast formation and osteoblast differentiation, thereby impacting chemokine release, matrix metalloproteinase activity, and bone mineral apposition—factors that contribute to the pathogenesis of inflammatory arthritis and osteoporosis. DR3 is also implicated in endothelial regulation through its ligand VEGI/TL1A, which restricts angiogenesis, and in tissues such as the aged bladder and leukemic cells where DR3 expression correlates with altered proliferation and inflammatory processes. These multifaceted actions highlight the therapeutic promise of targeting the TL1A/DR3 axis in a spectrum of inflammatory, degenerative, and neoplastic disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lei Fang, Becky Adkins, Vadim Deyev, et al. 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