(C4bC2b). The LP is similar to the CP; they share C3 convertase (C4bC2b). However, the LP does not rely on antibodies to identify pathogenic components but uses mannan binding lectin (MBL) and ficolins to identify sugars or N-acetylated groups on the surface of pathogens. In response, MBL-associated serine proteases (MASP1/MASP3 and MASP2) are activated [8]. The activated MASP1/MASP3 and MASP2 can cleave C2 and C4 to form C4bC2b [9,10]. The AP is different from the CP and LP; the AP is initiated by C3 itself. In the first step, the spontaneous hydrolysis of the thioester bond within C3 takes place, resulting in the formation of C3(H2O). Then, C3(H2O) recruits factor B (FB) to form a complex, which can be further cleaved by factor D (FD), leading to the formation of C3(H2O)Bb. C3(H2O)Bb is also a C3 convertase enzyme complex, which cleaves C3 to C3a and C3b. C3b can be added to FB and cleaved by FD, resulting in the formation of the C3 convertase C3bBb, which acts as an amplification loop of the complement system [11,12].
