“…Recently, TLRs were shown to be distributed in human uteroplacental tissues and when bound to their respective ligands, such as pathogen-associated molecular patterns (PAMPs) and endogenous danger-associated molecular patterns (DAMPS), trigger the activation of pro-inflammatory immune cells and production of pro-inflammatory cytokines [17,18]. Previous studies implicate viral infections to be associated with adverse pregnancy outcomes, which lead us to test whether viral infections play a role in development of preeclampsia [19,20]. Our previous studies reported that activation of TLR3, a double-stranded RNA receptor, with the double-stranded viral RNA mimetic polyinosinic:polycytidylic (poly I:C) caused inflammation, proteinuric hypertension, and endothelial dysfunction in rats and mice only if they were pregnant [21,11].…”