Results from studies in mice suggest that this pathogenesis is dependent on signaling through toll-like receptor 2 (TLR2), but not TLR4, although both TLR2- and TLR4-deficient mice can clear the infection as well as wild-type mice.14 Studies in humans and mice have shown that TLR2 is the primary pathogen-recognition receptor in the upper genital tract that drives the immune-pathogenic mechanisms associated with C. trachomatis infections.14,15. This evidence concerns the gene TLR4 and infection.