In physiological conditions, there is a delicate balance between complement activation and regulation. Insufficient regulation or excessive activation can result in a large variety of disorders [55]. The host expresses a variety of both fluid-phase and membranebound inhibitory proteins to regulate the location and activity of complement factors. Soluble inhibitors of the complement system include C1 inhibitor, C4 binding protein, factor I, factor H (FH), and MBL-associated protein of 44 kilodalton, which can be distributed throughout the body with the blood [56]. These soluble inhibitors have the characteristics of systematic regulation, which easily lead to immune regulation imbalance and lack of targeting. Membrane-bound inhibitory proteins are anchored on the membrane surface of specific cells to protect the host from complement attack. These membrane-bound inhibitors can be divided into two categories. The first includes inhibitors of the formation of C3 convertases, including CR1, decay accelerating factor, and membrane cofactor protein. Crry is expressed in rodents, which is similar to human CR1 in structure and function. The other is represented by CD59, which competes to combine with C8 and C9, further inhibiting MAC formation [57].
