Inflammation and oxidative stress at the maternal-fetal interface characterize 
the placental dysfunction that underlies the pregnancy disorder preeclampsia. 
Specialized fetal trophoblasts directly interact with leukocytes at both sites 
of the maternal-fetal interface; the uterine wall decidua; and the placenta. 
TLR3 has been implicated in the harmful inflammation at the maternal-fetal 
interface in preeclampsia, but the cellular involvement in the decidua and 
placenta has not been determined. This study aimed to characterize and quantify 
cell-specific TLR3 expression and function at the maternal-fetal interface in 
normal and preeclamptic pregnancies. TLR3 expression was assessed by 
immunohistochemistry and quantified by a novel image-based and cell-specific 
quantitation method. TLR3 was expressed at the maternal-fetal interface by all 
decidual and placental trophoblast types and by maternal and fetal leukocytes. 
Placental, but not decidual, TLR3 expression was significantly higher in 
preeclampsia compared to normal pregnancies. This increase was attributed to 
placental intravillous tissue and associated with both moderate and severe 
placental dysfunction. TLR3 pathway functionality in the decidua and placenta 
was confirmed by TLR3 ligand-induced cytokine response, but the TLR3 expression 
levels did not correlate between the two sites. In conclusion, functional TLR3 
was broadly expressed by maternal and fetal cells at both sites of the 
maternal-fetal interface and the placental intravillous expression was increased 
in preeclampsia. This suggests TLR3-mediated inflammatory involvement with local 
regulation at both sites of the maternal-fetal interface in normal and 
preeclamptic pregnancies.