Preeclampsia is a pregnancy-specific disorder, of which one of its major 
subtypes, the placental subtype is considered a response to an ischemic 
placental environment, impacting fetal growth and pregnancy outcome. 
Inflammatory immune responses have been linked to metabolic and inflammatory 
disorders as well as reproductive failures. In healthy pregnancy, immune 
regulatory mechanisms prevent excessive systemic inflammation. However, in 
preeclampsia, the regulation of immune responses is disrupted as a result of 
aberrant activation of innate immune cells and imbalanced differentiation of 
T-helper cell subsets creating a cytotoxic environment in utero. Recognition 
events that facilitate immune interaction between maternal decidual T cells, NK 
cells, and cytotrophoblasts are considered an indirect cause of the incomplete 
remodeling of spiral arteries in preeclampsia. The mechanisms involved include 
the activation of immune cells and the subsequent secretion of cytokines and 
placental growth factors affecting trophoblast invasion, angiogenesis, and 
eventually placentation. In this review, we focus on the role of excessive 
systemic inflammation as the result of a dysregulated immune system in the 
development of preeclampsia. These include insufficient control of inflammation, 
failure of tolerance toward paternal antigens at the fetal-maternal interface, 
and subsequent over- or insufficient activation of immune mediators. It is also 
possible that external stimuli, such as bacterial endotoxin, may contribute to 
the excessive systemic inflammation in preeclampsia by stimulating the release 
of pro-inflammatory cytokines. In conclusion, a disrupted immune system might be 
a predisposing factor or result of placental oxidative stress or excessive 
inflammation in preeclampsia. Preeclampsia can thus be considered a 
hyperinflammatory state associated with defective regulation of the immune 
system proposed as a key element in the pathological events of the placental 
subtype of this disorder.