Nomenclature: C57BL/6NTac-Trem2^em1(TREM2)

Taconic’s humanized TREM2 mouse model is designed to enable precise investigation of myeloid immune signaling in health and disease. TREM2 is a cell-surface receptor predominantly expressed on microglia in the central nervous system and macrophages in peripheral tissues, where it functions as a key regulator of innate immune activation. Through ligand recognition and downstream signaling via adaptor proteins such as DAP12, TREM2 influences microglial survival, proliferation, phagocytic activity, and inflammatory responses. 

The TREM2 receptor is critical for microglia responses to AD pathology. This humanized protein is fully functional (common variant) and can be used as a control for human risk variant models (e.g. R47H). When expressed/crossed with a pathogenic Alzheimer’s Disease (AD) model (e.g. Arte10), amyloid-β–induced microgliosis and microglial activation via its interactions with neurons and plaques can occur. Reference

Expression levels of TREM2 in the brain will be lower than those crossed to an AD pathogenic model.  Although human and murine TREM2 show identical functionality they have structural differences with ~77% sequence identity impacting amino acid variations, ligand binding, and disease relevance. These hTREM2 mice should have similar expression levels and patterns to WT mouse TREM2.

Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation. 

Recommended Controls

The recommended control for this model is C57BL/6NTac.

Origin

This model was developed by Taconic Biosciences through CRISPR/Cas9-mediated gene editing to replace the entire mouse Trem2 coding sequence with human TREM2 exons 1-5 beginning with the human TREM2 signal peptide. 

The human TREM2 gene is expressed under the control of the endogenous mouse Trem2 promoter and should thus recapitulate the expression pattern of the mouse Trem2 gene. Replacement of the mouse Trem2 gene with its human counterpart results in loss of function of the mouse Trem2 gene.