The tumor necrosis factor-alpha (TNF/TNF-α) gene encodes a pro-inflammatory cytokine belonging to the TNF superfamily. It is primarily produced by macrophages/monocytes during acute inflammation. TNF-α regulates immune cell function by binding to its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR, participating in normal inflammatory and immune responses. TNF-α is involved in various biological processes, including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This factor is associated with several diseases, such as autoimmune conditions, insulin resistance, psoriasis, rheumatoid arthritis, ankylosing spondylitis, tuberculosis, autosomal dominant polycystic kidney disease, and cancer. Mutations in the TNF-α gene impact susceptibility to cerebral malaria, septic shock, and Alzheimer’s disease ^[1-2]. In mice, defects in this gene are associated with impaired responses to bacterial infections, defects in the organization of follicular dendritic cell networks and germinal centers, and a lack of primary B cell follicles.

The huTNF(DBA/1) mice is a mouse Tnf gene humanized model. The mouse Tnf gene in the DBA/1 strain is replaced with the human TNF gene, including the 5’UTR and 3’UTR. This model is useful for diseases researches such as rheumatoid arthritis (RA). Since immunization of DBA/1 mice with type II collagen leads to severe polyarthritis mediated by the autoimmune response, DBA/1 mice are widely used for RA model construction. Therefore, huTNF(DBA/1) mice constructed on a DBA/1 strain background can be used to research immune-related diseases such as RA. In addition, based on the independently developed TurboKnockout fusion BAC recombination technology, Cyagen can also generate mutation models based on this strain and provide customized services.