Immune factors, such as auto-antibodies, oxidative
stress and natural killer (NK)-cell abnormalities,
cause placental dysfunction and impaired placental
perfusion. The latter acts as a stimulus of placental
release of anti-angiogenic and inflammatory mediators
that eventually cause endothelial dysfunction
and organ damage.58 Increased numbers of activated
monocytes and macrophages have been described
in the endometrium of women with PE.59 A misbalance
between antioxidant and pre-oxidant factors
and increased production of ROS results in vascular
endothelium dysfunction in women with PE.60 One
study showed that women with early-onset severe
preeclampsia have increased NK cell function related
to cytokine production