TNFRSF1B Specific Neutra™ Antibody Products

TNF receptor superfamily member 1B (TNFRSF1B), also known as TNFR2 or CD120b, is a cell surface receptor involved in tumor necrosis factor-alpha (TNFα) signaling. It is a type I transmembrane protein and consists of extracellular cysteine-rich domains responsible for ligand binding, a transmembrane domain, and intracellular regions mediating downstream signaling. TNFRSF1B is expressed on various cell types, such as immune cells, neurons, and endothelial cells. Its activation regulates immune responses, inflammation, and cell survival, contributing to the pathogenesis of many illnesses.

Its Gene ID: 7133, UniProtKB ID: P20333, and OMIM ID: 191191.

TNFRSF1B Signal Pathways

TNFRSF1B is one of the important receptors for TNFα. TNFRSF1B interacts with TNFα, initiating downstream signaling cascades crucial for immune regulation and inflammation. When TNFRSF1B is activated by TNFα, its intracellular domain recruits TRAF2/cIAP1/cIAP2 complexes, triggering both canonical and non-canonical NF-κB activation. The PI3K/Akt pathway can also be activated reciprocally. Besides, p38 MAPK will be activated in macrophages and murine B cells upon TNFRSF1B stimulation. These result in the transcriptional regulation of genes implicated in inflammation, apoptosis, and cell survival.

Fig.1 TNFR2 (TNFRSF1B) signaling pathways involved in various processes of tumor development.¹

TNFRSF1B in Tregs

TNFRSF1B is highly expressed in regulatory T cells (Tregs) and plays a crucial role in their functional maintenance. TNFRSF1B signaling in Tregs is essential for their suppressive function and stability. TNFRSF1B also can efficiently increase Tregs' proliferation and survival. Studies have shown that TNFRSF1B deficiency results in decreased suppressive activity of Tregs and impaired tolerance induction. The presence of high Tregs, particularly TNFRSF1B+ Tregs, in tumor microenvironments is linked with a poor prognosis in a variety of cancers.

TNFRSF1B Related Diseases

As the neuroprotective role of TNFRSF1B, increased levels of soluble TNFRSF1B can lead to schizophrenia. Additionally, TNFRSF1B dysfunction is linked to inflammatory conditions like systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel disease, where aberrant TNFRSF1B signaling exacerbates inflammation and tissue damage. Moreover, TNFRSF1B has been implicated in cancer progression, with its overexpression promoting tumor growth and immune evasion in certain malignancies. The expression of TNFRSF1B is found to increase in various cancers, like breast cancer, and colon cancer. The expression of TNRF2 in tumor cells has also been linked to late-stage cancer.

Antibodies Targeting TNFRSF1B

Antibodies targeting TNFRSF1B work in a variety of ways to treat disease. In cancer, TNFRSF1B antagonistic antibodies inhibit TNFα-mediated tumor growth by blocking TNFRSF1B signaling, thereby impeding tumor cell proliferation and survival. Additionally, they enhance anti-tumor immunity by promoting tumor cell recognition and elimination, modulating immune cell function, such as Impairment of Tregs function, relief of Tregs-mediated immune suppression, and stimulation of cytotoxic CD8 T cell activation. In inflammatory diseases, by enhancing Treg function and suppressing effector T cell activation, TNFRSF1B agonist antibodies restore immune balance, thereby mitigating inflammation and tissue damage. This dual mechanism of action underscores the therapeutic potential of TNFRSF1B antibodies in tumor immunotherapy and inflammatory disorders, offering promising avenues for clinical intervention.

Fig.2 Effect of TNFR2 (TNFRSF1B)-targeting agents on the activity of Tregs.²

Creative Biolabs offers seven kinds of high-quality, reproducible anti-TNFRSF1B antibody products to help you complete your research more efficiently.

REFERENCES

1. Li, Muchun, et al. "Targeting TNFR2: A novel breakthrough in the treatment of cancer." Frontiers in Oncology 12 (2022): 862154. Distributed under Open Access license CC BY 4.0, without modification.
2. Zou, Huimin, et al. "Modulation of regulatory T cell activity by TNF receptor type II-targeting pharmacological agents." Frontiers in immunology 9 (2018): 594. Distributed under Open Access license CC BY 4.0, without modification.