Complement activation is a key part of the innate immune system, which plays a crucial role in the defense against microbial infections, healing of the host, and disposal of the products of inflammatory injury [1-3]. The complement system consists of complement components, receptors, and regulatory factors. Most of the serum complement components are produced in the liver, and many complement receptors (CRs) are expressed in liver Kupffer cells and hepatic stellate cells [4-6]. According to the recognition of different molecules, complement activation can be divided into three main pathways: the classical pathway (CP), the alternative pathway (AP), and the lectin pathway (LP) (Fig. 1) [7]. The CP is triggered by C1q recognition of antibodies bound to antigens or microbial surfaces, resulting in the activation of C1r and C1s. The activated C1s then cleaves C4 and C2 to form C3 convertase (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
