Anti-Mouse TREM2 (178) In Vivo Antibody - LALAPG (ICH1262LALAPG-50mg)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

This is a mouse IgG2a-format monoclonal antibody, clone 178, directed against mouse TREM2, carrying a LALAPG (L234A/L235A/P329G) Fc mutation. The LALAPG substitutions abolish binding to activating Fc-gamma receptors and C1q, producing an effector-silenced ("Fc-dead") antibody that engages and blocks its target without triggering ADCC, ADCP, or complement-dependent cytotoxicity. This design is well suited to studies that need to interrogate TREM2 receptor blockade and signaling per se, cleanly separating the contribution of ligand/signal neutralization from Fc-mediated cell depletion. It is validated for blocking, ELISA, functional assays, flow cytometry, and in vivo use. Supplied at low endotoxin (research grade less than 1 EU/mg; ultra-low grade less than 0.5 EU/mg), in an in-vivo-ready buffer, and available in bulk milligram-to-gram quantities. For research use only. Researchers typically identify this reagent by its clone designation, 178, which is a widely referenced anti-mouse TREM2 clone in myeloid and tumor immunology work. TREM2 (Triggering Receptor Expressed on Myeloid cells 2; UniProt Q99NH8, also called PLOSL2) is a single-pass transmembrane immunoreceptor of the immunoglobulin superfamily expressed predominantly by myeloid cells, including microglia, osteoclasts, dendritic cells, and tissue and tumor-associated macrophages. Lacking its own signaling motifs, TREM2 pairs with the adaptor DAP12 (TYROBP) to transduce signals via SYK and downstream PI3K/AKT and other pathways. It recognizes a broad range of ligands, notably anionic lipids, lipoproteins, phospholipids, and apoptotic-cell surfaces. Functionally, TREM2 promotes phagocytosis, cell survival and proliferation, lipid sensing and metabolism, and anti-inflammatory or reparative macrophage programs. TREM2 is central to microglial biology in neurodegeneration and, in cancer, marks immunosuppressive tumor-associated macrophage states that restrain T-cell and NK-cell antitumor immunity, making it a target of active investigation across neuroimmunology, metabolic disease, and tumor immunology.