Toll-Like Receptor 3 Deficiency Leads to Altered Immune Responses to Chlamydia trachomatisInfection in Human Oviduct Epithelial Cells

Reproductive tract pathology caused by Chlamydia trachomatisinfection is an important global cause of human infertility. To better understand the mechanisms associated with Chlamydia-induced genital tract pathogenesis in humans, we used CRISPR genome editing to disrupt Toll-like receptor 3 (TLR3) function in the human oviduct epithelial (hOE) cell line OE-E6/E7 in order to investigate the possible role(s) of TLR3 signaling in the immune response to Chlamydia.