Tnfrsf1b, also known as tumor necrosis factor receptor superfamily member 1B, encodes tumor necrosis factor receptor 2 (TNFR2), one of the two receptors for cytokines TNF and lymphotoxin-α [4]. TNFR2 has both pro-and anti-inflammatory effects and is involved in various biological processes like immune regulation, protecting cells such as oligodendrocytes, cardiomyocytes, and keratinocytes [4].

In ovarian cancer, single-cell RNA sequencing identified a novel exhausted subpopulation of CD8+ TNFRSF1B+ T cells associated with poor survival. Blockade of TNFRSF1B inhibited tumor growth by remodeling the immune microenvironment [1].

In cutaneous melanoma, TNFRSF1B gene variants c.587T>G and c.*922C>T were independent prognostic factors [2].

In inflammatory bowel disease, lncRNA NEAT1 promoted NF-κB p65 translocation and mediated intestinal inflammation by regulating TNFRSF1B [3].

In hepatocellular carcinoma, mucosal-associated invariant T (MAIT) cells secreted TNF to activate TNFRSF1B on regulatory T cells, promoting immunosuppression [5].

In conclusion, Tnfrsf1b plays crucial roles in multiple diseases including ovarian cancer, cutaneous melanoma, inflammatory bowel disease, and hepatocellular carcinoma. Its functions range from immune regulation in the tumor microenvironment to mediating inflammatory responses. Studies on Tnfrsf1b using in vivo models have provided insights into its role in disease development, offering potential therapeutic targets for these diseases.