Now ask it to write a bodice-ripper & post the results. ;-)
Results:
A schematic overview of three activation pathways of the complement system is outlined in Figure 1. Regardless of the activation pathway, the enzymatic cascade generates C3 convertase, which cleaves the most abundant C3 protein, into C3b and C3a. As the key effector molecule of the complement system, C3b and its inactive fragment iC3b bind covalently to the cell membrane and opsonize the antigen for eventual phagocytosis. Subsequently, C3b binds to C3 convertase to form C5 convertase that generates C5b and C5a. The assembly of the terminal complement proteins (C5b, C6, C7, C8, C9) contributes to the formation of the membrane attack complex (MAC) that disrupts the cellular lipid bilayer of the extracellular materials including bacteria, viruses, and nanocarriers. Meanwhile, C3a and C5a act as potent inflammatory mediators [11]. The detailed mechanisms of the complement system are not within the scope of this paper, yet there are several excellent literature reviews focusing on this subject [21,32,33,34].