TREM-1 Protein, Mouse (HEK293, His)

TREM-1, a cell surface receptor, assumes pivotal roles in both innate and adaptive immunity by robustly amplifying inflammatory responses. Upon activation by diverse ligands such as PGLYRP1, HMGB1, or HSP70, TREM-1 undergoes multimerization and forms a complex with the transmembrane adapter TYROBP/DAP12. This initiates a SYK-mediated cascade of tyrosine phosphorylation, activating downstream mediators like BTK, MAPK1, MAPK3, or phospholipase C-gamma. Consequently, this cascade facilitates the release of pro-inflammatory cytokines and/or chemokines by neutrophils and macrophages, promoting their migration and thereby amplifying inflammatory responses triggered by bacterial and fungal infections. Beyond microbial interactions, TREM-1 also contributes to the amplification of inflammatory signals initiated by Toll-like receptor (TLR) and NOD-like receptor engagement, playing a crucial role in the pathophysiology of various acute and chronic inflammatory diseases, including septic shock and atherosclerosis. In its monomeric state, TREM-1 forms homomultimers upon activation and interacts with TYROBP/DAP12 and TLR4, further highlighting its intricate involvement in the regulation of immune responses.