{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTREM‐1 is a transmembrane receptor prominently expressed on myeloid cells—including neutrophils, monocytes, dendritic cells, microglia, and others—and serves as a potent amplifier of inflammatory responses. Its engagement, often following Toll‐like receptor stimulation by microbial products, triggers robust production of pro‐inflammatory cytokines and chemokines, enhances degranulation and respiratory burst in neutrophils, and even promotes dendritic cell maturation. TREM‐1 expression is rapidly up‐regulated upon exposure to bacterial components, and its soluble form (sTREM‐1) is generated by metalloproteinase‐mediated cleavage, serving both as a modulator of inflammation and a diagnostic biomarker. Moreover, transcriptional regulation by NF‐κB positively regulates TREM‐1 while factors such as PU.1 and aging can down‐modulate its signaling, contributing to states like endotoxin tolerance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, TREM‐1 functions by partnering with the ITAM‐bearing adaptor DAP12 to initiate intracellular signaling cascades—including activation of ERK, p38 MAPK, and NF‐κB—that synergize with TLR‐derived signals. In addition to microbial ligands, endogenous molecules (such as the peptidoglycan recognition protein–peptidoglycan complexes and the recently identified extracellular cold‐inducible RNA‐binding protein) can serve as TREM‐1 ligands, thereby linking danger signals to inflammatory amplification. TREM‐1 signaling is further modulated by regulatory proteins and environmental conditions; for instance, its expression is enhanced under hypoxic conditions in dendritic cells yet can be counterbalanced by inhibitory adaptors like NTAL. In ocular and periodontal contexts, engagement of TREM‐1 intensifies cytokine production and inflammatory mediator release, while comparative studies with related receptors (e.g., TREM‐2) underscore a complex interplay that finely tunes immune activation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in host defense, dysregulated TREM‐1 activity has been implicated in a broad spectrum of pathological conditions. Aberrant TREM‐1 signaling contributes to immunosuppression and therapeutic resistance in tumor microenvironments (as seen in hepatocellular carcinoma and prostate cancer), promotes atherosclerotic lesion development under dyslipidemic conditions, and is linked to tissue damage and fibrogenesis in organs such as the liver and kidney. Elevated sTREM‐1 levels have been associated with acute inflammatory states including sepsis, pneumonia, ventilator‐associated pneumonia, and chronic inflammatory lung diseases like COPD, while increased TREM‐1 expression is also observed in inflammatory conditions ranging from ocular keratitis and periodontal disease to preeclampsia. These diverse observations underscore the potential of targeting TREM‐1 therapeutically to recalibrate inflammatory responses in both infectious and non‐infectious diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Richard J N Allcock, Alexander D Barrow, Simon Forbes, et al. 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