SLC35A2 and chlamydia infectious disease: Collectively, our data indicate that TLR3 deficiency results in a more rapid breakdown in epithelial barrier function during Chlamydia infection, and proposes the hypothesis that Chlamydia exploits this phenomenon during TLR3 deficiency as a mechanism to accelerate its rate of ascent into the UGT of female mice early during infection (Fig 1) and causing increased pathology relative to WT mice [27].