{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nLIGHT (TNFSF14) is a multifunctional cytokine of the tumor necrosis factor superfamily that critically regulates immune responses. Expression of LIGHT on activated T lymphocytes and natural killer cells provides potent costimulatory signals that enhance T‐cell activation and Th1 cytokine production, and, together with its soluble receptors, modulates regulatory T‐cell functions. In animal models, constitutive LIGHT expression in T cells perturbs lymphoid architecture and elicits robust mucosal inflammation resembling Crohn’s disease and other autoimmune conditions, while NK cell–derived LIGHT promotes dendritic cell maturation to help bridge innate and adaptive immunity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nLIGHT can also influence cell survival and death in a context‐dependent manner. On one hand, LIGHT sensitizes several tumor cell types to interferon‐γ–mediated, caspase‐dependent apoptosis in colon and breast cancer models and, through its release on tumor‐derived microvesicles, modulates T‐cell responses against melanoma. Conversely, in primary hepatocytes LIGHT can activate NF‑κB–dependent anti‐apoptotic pathways that protect cells from TNFα‐induced apoptosis. These seemingly divergent effects underscore a dual role for LIGHT in tumor immunosurveillance and the regulation of apoptosis in both malignant and nontransformed tissues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in immune cell activation and apoptosis, LIGHT profoundly affects the tissue microenvironment by regulating stromal and vascular cell function, fibrosis, and osteoclastogenesis. LIGHT released from platelets and other cellular sources induces proinflammatory and prothrombotic responses in endothelial cells via activation of NF‑κB and STAT3 signaling, upregulating adhesion molecules and chemokines. In models of metabolic and fibrotic disease, LIGHT drives the formation of tertiary lymphoid organs, skin and lung fibrosis, and bone destruction in multiple myeloma and metastatic lesions; it modulates keratinocyte proliferation and the expression of matricellular proteins in atopic dermatitis and scleroderma, influences fibroblast function in eosinophilic esophagitis, and is emerging as a biomarker in conditions ranging from coronary artery disease to COVID‑19 cytokine release syndrome. 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