Toll-like receptor 3 (TLR3) is a crucial immune system receptor, encoded by the TLR3 gene. TLR3 is a member of the Toll-like receptor family, which plays a foundational role in pathogen recognition and the activation of innate immune responses. TLR3 primarily recognizes double-stranded RNA (dsRNA), a common feature of the viral genomes internalized by macrophages and dendritic cells during viral infections. TLR3, through the adapter TRIF/TICAM1, leads to the activation of NF-κB, nuclear translocation of IRF3, secretion of cytokines, and inflammatory responses. Therefore, TLR3 plays a role in host defense against various viruses. In addition, the research progress of TLR3 in respiratory diseases has also attracted attention. For example, TLR3 also plays an important role in airway immune responses, inflammation regulation, airway remodeling, tumor occurrence and metastasis. Therefore, the role of TLR3 in the occurrence and development of recurrent respiratory infections has also become a current research hotspot.

This strain is a Tlr3 gene knockout (Tlr3 KO) mouse, which uses gene editing technology to knock out the Tlr3 gene in mice homologous to the human TLR3 gene. Homozygous Tlr3 KO mice are viable and fertile. Research shows that, unlike the macrophages of wild-type mice, the macrophages of Tlr3 KO mice cannot produce the inflammatory cytokines IFN-α or IFN-β when attacked by polyinosinic-polycytidylic acid. Primary splenocytes isolated from homozygous Tlr3 KO mice are unresponsive to viral dsRNA and have reduced IL-6 production.