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.