Because IFN-γ, TNFα, and IL-1β are all differentially expressed in the context of TLR3 deficiency in murine OE cells and mice [8, 27], we hypothesized that TLR3 deficiency might have a significant impact on the integrity of the epithelial barrier within the female reproductive tract during Chlamydia infection, due to the altered expression of these and other key cytokines. Here, TLR3 is linked to chlamydia infectious disease.