TREM receptor

The Triggering Receptor Expressed on Myeloid cells (TREM) family consists of several receptors expressed on the surface of myeloid cells, among which TREM-1 and TREM-2 are the most extensively studied. TREM-1 acts as an amplifier of immune responses, significantly enhancing the responses of macrophages and neutrophils to bacteria and fungi, and promoting the release of inflammatory cytokines such as TNF-α and IL-1β, thus playing a crucial role in acute inflammation and infection responses. Modulating TREM-1 signaling can alleviate the severity of sepsis. TREM-2 helps regulate immune responses by promoting the anti-inflammatory and repair functions of macrophages, maintaining tissue stability, particularly in neural tissues, where the function of TREM-2 is closely associated with slowing the progression of neurodegenerative diseases like Alzheimer’s disease.
The Triggering Receptor Expressed on Myeloid cells interacts with its adaptor protein DAP12 to initiate signaling pathways, including those involving the tyrosine kinase Syk, which in turn activates a variety of downstream cellular responses, including the production of inflammatory cytokines, enhancement of cell survival signals, and reorganization of the cytoskeleton. The Triggering Receptor Expressed on Myeloid cells and their adaptor proteins are not only crucial for understanding immune regulation mechanisms but also provide new targets for the study of various diseases, including inflammatory and neurodegenerative diseases^[1].