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.