The maternal inflammatory response to pregnancy

It is generally believed that successful pregnancy is biased towards Th2 immunity, while pathological pregnancies, such as pre-eclampsia, are characterized by cell-mediated (Th1) immunity. However, it is increasingly apparent that the Th1/Th2 paradigm is too simplistic, as normal human pregnancy is also associated with activation of the innate immune system to give an inflammatory response, both locally in the decidua in early pregnancy and systemically throughout gestation. The systemic inflammatory response is exaggerated in pre-eclampsia. Our recent evidence suggests that this inflammatory response is mediated through the innate immune system (monocytes and NK cells) in response to syncytiotrophoblast debris shed into the maternal circulation. We propose that the activation of type I immunity in pre-eclampsia is due to stimulation of the maternal innate immune system by syncytial debris altered by oxidative stress, rather than activation of maternal T cells by fetal (paternal) antigens.