Toll-like receptor 4 (TLR4), encoded by the human TLR4 gene, is a type I transmembrane protein primarily expressed in monocytes and macrophages. As a crucial component of the innate immune system, TLR4 recognizes pathogen-associated molecular patterns (PAMPs) from microorganisms and damage-associated molecular patterns (DAMPs) from injured tissues. Its main function involves detecting lipopolysaccharides (LPS) from Gram-negative bacteria and initiating intracellular signaling via NF-κB or JNK/SAPK pathways. Additionally, TLR4 recognizes other PAMPs such as lipoteichoic acid (LTA) and double-stranded RNA (dsRNA), playing a pivotal role in the activation of innate immune responses. Research has demonstrated that TLR4 is involved in inflammation, antiviral defense, tumor therapy, and immune regulation. Upon activation, TLR4 triggers downstream signaling pathways, leading to the secretion of cytokines, type I interferons, and other pro-inflammatory mediators critical for innate immune responses.

This strain is a Tlr4 knockout (Tlr4 KO) mouse model utilizing gene editing technology to knock out the Tlr4 gene homologous to the human TLR4 gene in mice. Homozygous Tlr4 KO mice are viable and fertile and exhibit a variety of phenotypes associated with immune responses, including hyporesponsiveness to bacterial lipopolysaccharide (LPS) and elevated levels of respiratory syncytial virus.