TREM-1

TREM-1 (Triggering Receptor Expressed on Myeloid Cells-1) is an immunoglobulin superfamily receptor predominantly expressed on myeloid cells, where it functions as a potent amplifier of innate inflammatory responses through activation of monocytes, macrophages, and neutrophils^[1][2]. Mechanistically, TREM-1 cooperates with pattern-recognition receptor pathways and amplifies signals induced by NACHT-LRR (NLR) receptors, thereby promoting inflammatory cytokine production and downstream immune activation^[2]. Through this signaling function, TREM-1 acts as a central regulator of inflammation in both infectious and sterile disease settings, including sepsis, inflammatory disorders, cardiovascular disease, neuroinflammatory conditions, and multiple cancers^[1][3][4]. In disease models, dysregulated TREM-1 signaling contributes to pathological inflammatory amplification, while modulation of the pathway alters disease progression and immune responses^[1][3][4]. Compared with related members of the TREM family, TREM-1 is primarily characterized as a pro-inflammatory receptor that enhances myeloid-cell activation rather than mediating the specialized microglial functions commonly associated with TREM-2, making TREM-1 a distinct target for studies of innate immune amplification^[2]. For experimental applications, TREM-1 inhibition using peptide antagonists such as LP17 has been reported to reduce inflammatory pathology and tissue damage in preclinical models, whereas agonistic anti-TREM-1 antibodies have been used to investigate host-defense mechanisms, microbial clearance, and immune regulation in inflammatory disease models^[1][5]. These characteristics have established TREM-1 as a widely studied molecular target for mechanistic investigation and therapeutic intervention in inflammation-driven diseases^[1][3][4].