Tlr2 Conditional Knockout mouse models

Encoding a broadly promiscuous pattern recognition receptor, Tlr2 is the mouse ortholog of human TLR2 and uses a horseshoe of leucine-rich repeats with a hydrophobic pocket at the boundary of its central and C-terminal regions to sense bacterial lipoproteins, lipoteichoic acid, peptidoglycan fragments, zymosan, and fungal and parasitic lipids, always as a heterodimer with TLR1 or TLR6 and often assisted by CD14, CD36, or integrin beta 3. Ligand engagement dimerizes the TIR domains, recruits TIRAP and MyD88, and activates IRAK and TRAF6 for NF-kB and MAPK output, with a minor endosomal interferon component. Nulls are viable and highly informative in infection models, so germline deletion is a reasonable default, conditional alleles separate myeloid, epithelial, and astrocyte sensing, and ectodomain humanization supports antagonists that fail to cross-react. Because Tlr1 and Tlr6 partition ligand classes, interpret co-receptor genetics together and target clearance, sterile inflammation, or adjuvant endpoints.

Tlr2 conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype.