Abstract: The early phase of pregnancy is characterized by an inflammatory-like process
and vascular remodeling that occur in decidua and are associated with hormonal changes.
Extravillous trophoblast and NK cells present in decidua are responsible for these changes
that are also contributed by the complement system. Complement activation occurs in
physiologic pregnancy at decidual level as a result of tissue remodeling. Soluble and cell
surface expressed complement regulators protect decidual endothelial cells (DECs) and
trophoblast from complement attack that may lead to tissue damage in normal pregnancy.
The recent report that preeclampsia is associated with mutations in the genes encoding for
some of the complement inhibitors supports the important role of these proteins in the
protection of the feto-placental unit. Control of complement activation can easily be
overcome in the presence of complement-fixing antibodies directed against β2-
glycoprotein I responsible for fetal loss and growth restriction.
Complement components synthesized by several decidual cells including trophoblast,
DECs, and macrophages serve a defense function against infectious agents and
promotes the removal of apoptotic cells. More, the complement system was recently
found to contribute to placental development. Particularly important in this regard is
C1q which is expressed on the surface of DECs and acts favoring the adhesion of
endovascular trophoblast to the endothelial cells. Extravillous trophoblast is another
source of C1q which binds to extracellular matrix and promotes trophoblast migration
through the decidua. Unremodeled spiral arteries are surrounded by trophoblast cells
that manifests reduced expression of C1q with important implications in preeclampsia
characterized by reduced vascular remodeling.
