Invivo Anti-Mouse TNFR2 (CD120b) Recombinant mAb

TNFR2, or tumor necrosis factor receptor 2 (encoded by the TNFRSF1B gene), is a type I transmembrane glycoprotein of approximately 75 kDa belonging to the TNF receptor superfamily. It is primarily expressed on the surface of immune cells (such as Treg cells, myeloid-derived suppressor cells or MDSCs, endothelial cells, and certain tumor cells). Unlike the ubiquitously expressed TNFR1, TNFR2 exhibits higher affinity for its ligand TNF-α but is only efficiently activated when high concentrations of TNF-α are present in specific microenvironments (such as inflammatory or tumor microenvironments). Functionally, TNFR2 not only participates in classical pro-inflammatory signaling (by recruiting adaptor proteins such as TRAF2 to activate NF-κB and PI3K/AKT pathways, promoting cell survival, proliferation, and angiogenesis) but also plays a "double-edged sword" role in immune regulation: on one hand, TNFR2 is a critical receptor for maintaining Treg cell stability and suppressive function, as its signaling promotes Treg expansion and enhances their immunosuppressive capacity; on the other hand, within the tumor microenvironment, TNFR2 highly expressed on tumor cells—upon binding TNF-α—promotes tumor invasion and metastasis through the NF-κB pathway, while TNFR2 on tumor-infiltrating Tregs exacerbates local immunosuppression, and TNFR2 on MDSCs promotes their accumulation and suppressive activity. Furthermore, TNFR2 has been recognized as a "survival switch" for tumor cells to evade T-cell killing—by inducing anti-apoptotic protein expression to resist TNF-mediated cytotoxicity. Given its dual pivotal roles in immunosuppression and tumor survival, TNFR2 has emerged as a prominent novel immunotherapy target following PD-1/PD-L1, with various anti-TNFR2 agonistic antibodies (for activating Tregs to treat autoimmune diseases) and antagonistic antibodies (for blocking tumor immunosuppression) currently in preclinical and early-stage clinical development, aiming to achieve precise regulation of immune responses for therapeutic purposes.