{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTNFRSF14, also known as herpesvirus entry mediator (HVEM), is a multifunctional member of the tumor necrosis factor receptor superfamily that orchestrates the balance between immune activation and inhibition. Structural and biochemical studies have revealed that its extracellular domain engages a diverse set of ligands—including the TNF‐related cytokine LIGHT as well as the immunoglobulin superfamily members BTLA and CD160—to mediate bidirectional signaling. This receptor not only triggers costimulatory pathways (for example, inducing NF‐κB activation via LIGHT binding) but also dampens immune responses when interacting with inhibitory ligands. In addition, TNFRSF14 serves as a critical receptor for herpes simplex virus glycoprotein D, thereby facilitating viral entry and subsequent downstream signaling events."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThrough its capacity to interact with both activating and inhibitory ligands, TNFRSF14 functions as a molecular switch in immune regulation. Engagement with LIGHT promotes cell survival and activation via NF‐κB and other downstream pathways—thereby enhancing T cell and natural killer cell responses—whereas binding to BTLA or CD160 transmits inhibitory signals that limit excessive inflammatory activity. Furthermore, by forming distinct cis or trans complexes, TNFRSF14 finely tunes lymphocyte activation and contributes to the maintenance of immune homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic studies and expression analyses have implicated TNFRSF14 in a broad range of pathological conditions. Genome‐wide association studies have linked variants at the TNFRSF14 locus with susceptibility to autoimmune diseases such as rheumatoid arthritis, and somatic mutations or deletions in TNFRSF14 are frequently detected in lymphomas (for example, pediatric‐type follicular lymphoma), where they correlate with poor clinical outcomes. In solid tumors—including colorectal, hepatocellular, esophageal, and bladder cancers as well as glioblastoma—altered TNFRSF14 expression has been associated with impaired apoptotic responses and aberrant proliferation, while in chronic lymphocytic leukemia TNFRSF14 signaling can promote tumor cell death. Collectively, these findings underscore the diverse roles of TNFRSF14 in tumor suppression, immune surveillance, and cell fate determination."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in immune cell signaling and tumor biology, TNFRSF14 influences inflammatory processes and homeostasis in barrier tissues. Activation of TNFRSF14 by LIGHT in endothelial cells stimulates the secretion of proinflammatory chemokines, while in keratinocytes, engagement of TNFRSF14 regulates cellular proliferation and the expression of matricellular proteins such as periostin—factors that contribute to the development of conditions like atopic dermatitis. These findings further attest to the pleiotropic nature of TNFRSF14 in integrating immune signals with tissue-specific responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "John R Sedy, Maya Gavrieli, Karen G Potter, et al. 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