Moreover, excessive CSF1-driven accumulation of decidual macrophages at the fetal-maternal interface can be prevented by the high constitutive decidual MIF levels, resulting in tight control of the decidual macrophage population that could have an impact on fertility and pregnancy maintenance.
Previous studies have shown that pre-eclampsia is associated with augmented expression of TNF and IL1B and excess decidual macrophage infiltration.
CSF1 levels are elevated in the blood of patients prior to the onset of preeclamptic signs or symptoms. Furthermore, increased CSF1 expression has been reported in placental tissue obtained from pre-eclamptic patients. Consequently, the induction of CSF1 by TNF and IL1B during the period of endovascular trophoblast invasion may promote the infiltration of macrophages. The presence of the latter in the placental bed may be a source of TNF, which induces apoptosis in extravillous trophoblasts and restricts their invasion. The resulting shallow placentation is a hallmark of pre-eclampsia. Similarly, we have reported that TNF and IL1B also induce the expression of another macrophage chemoattractant, monocyte chemoattractant protein-1, in cultured DCs.