Tumor necrosis factor receptor type II (TNFR2)

Tumor necrosis factor receptor type II (TNFR2) is a transmembrane receptor belonging to the TNF receptor superfamily, encoded by the TNFRSF1B gene. It primarily binds the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) and is characterized by four extracellular cysteine-rich domains, but lacks the death domain found in TNFR1. TNFR2 expression is restricted mainly to immune cells (including regulatory and effector T cells, myeloid cells, and some B cells), certain tumor cells, and a few non-immune cells such as endothelial and neural cells. TNFR2 mediates both pro-inflammatory and anti-inflammatory effects: it regulates the function, stability, and proliferation of T regulatory cells (Tregs), drives immune suppression within the tumor microenvironment, and plays roles in both tumorigenesis and autoimmune regulation. It acts as a key modulator of the balance between immune activation and tolerance. TNFR2 is emerging as a promising therapeutic target, with antagonists and agonists in development for cancer, autoimmune diseases, and inflammatory disorders. Its biological and clinical significance is defined by its complex pleiotropic effects on immune regulation, cell death, and tumor progression[1][2][3][5][7].

Other names

Tumor necrosis factor receptor superfamily member 1BTNFRSF1BCD120bTNF receptor type IITNF-R2

Antagonists block TNFα-TNFR2 interaction to reverse immune suppression, enhance antitumor immunity, or suppress regulatory T cell function[3][5]; Agonists activate TNFR2 to promote regulatory T cell expansion and immune modulation in autoimmune or inflammatory settings[3]; Immunomodulation through selective regulation of Treg, myeloid-derived suppressor cell (MDSC), and effector T cell responses[3][5]