Supportive evidence comes from our findings that TLR3/7/8 immunoreactivity and mRNA levels are increased significantly in placentas of women with PE, that direct activation of TLR3/7/8 occurs in human trophoblasts, and that TLR3/7/8 activation in mice causes placental inflammation, splenomegaly, fetal demise, and pregnancy-dependent hypertension and endothelial dysfunction. Here, TLR3 is linked to endothelial dysfunction.