Introduction
The complement system is a huge family comprised of more than 50 proteins. They play an important role in removing non-self or modified-self danger signals. The complement system is canonically regarded as the first chemical barriers to defend against microorganism infection. Complement effectors can induce inflammation and adaptive immune activation 1. And it intertwines with other crucial pathways like Toll-like receptor (TLR) signaling pathway2 and the coagulation pathway 3. Clearly, they must be carefully controlled. If it fails, complement can target on host tissue and cause damage to it. Aberrant complement activation leads to “thrombo-inflammation” attacks to placenta and destroy the structure and function of it, thus leading to many pregnancy disorders. Studies have indicated that dampening complement activation can ameliorate pregnancy outcomes 4-5.
Although aberrant complement activation is related to many pathological pregnancy events, now large amount of immunological and histological evidences show that complement proteins and its split products are also significantly increased in physisological pregnancy. Placenta (like stromal cells, trophoblasts, endothelial cell, immune cells) synthesize complement proteins in a context-driven (hormone and immune micro-environment) manner and complement activation fragments increased locally and systematically6. These changes of complement system may adapt to meet the need of our body during pregnancy.