Physiological complement activities in placenta structure and
immune homeostasis
Cell apoptosis in placentation
A total reconstruction on maternal-fetal interface takes place during
placenta development. Trophoblast invade into the decidual, accompanied
by the replacement of maternal decidual and the generation of the new
tissue, a so called “remodeling” procedure. It has been found that the
proliferation and apoptosis of trophoblast are stay in balance in the
process of placentation. Apoptosis is a normal physiological phenomenon
throughout gestation period. Whole data indicated that apoptosis is
important in placenta development, remodelling and
function22.
In physical condition, dying cells can be recognized by a series of
molecules, which lead to their phagocytosis by immune cells or even its
neighboring cells. The removal of apoptotic cells is so rapid that few
cells are seen in tissues even in thymus where up to 95% of its cells
undergo apoptosis procedure. Timely clearance of dying cell is a crucial
for tissue homeostasis, since these cells are a main source of
self-antigens which can stimulate adaptive immunity activation and mount
a pathologic response to host tissue under inflammatory conditions.
Therefore, the carefully and precisely regulated clearance of apoptosis
cell involves in maintaining an anti-inflammatory and self-tolerance
state.
The trophoblasts invade and replace the maternal decidua tissue,
generating a large number of sub-cellular debris and apoptotic cells.
They accumulate in placenta and even deported into maternal circulation
in large quantities. They need to be cleared rapidly to prevent the
release of intracellular cytotoxic substances to the extracellular
microenvironment23. An unbalance of cell apoptosis
result in sever inflammation, placenta vascular
damage23, altered trophoblast function. When these
cell wastes shedding into the maternal blood-circulation, systematic
vascular damage and dysfunction happens. (Figure 2) These changes were
found in pathological pregnancy like intrauterine growth retardation and
pre-eclampsia22.