The complement system in fish consists of a series of proteins interacting with both the innate and the adaptive immune systems. These distinct plasma proteins sequentially react with one another whereby they eventually directly kill the pathogens. The system is activated by binding of complement factors to surfaces of invading pathogens. During this process, complement factors and their cleavage products may opsonize invading microorganisms, induce a series of inflammatory responses and finally kill the pathogens. Activation of the complement system may take place through three pathways called the classical pathway (CP), the alternative pathway (AP) and the mannan-binding pathway (or lectin pathway) (LP). These activation routes depend on the different molecules acting in the initiation of the sequential reactions but they all converge to activate the same central effector molecule, C3. This is achieved by formation of a C3 convertase. Activation of C3 leads to the formation of two fragments C3a (an important factor, together with C5a, for inducing inflammation via its effect as an anaphylatoxin) and C3b which facilitates phagocytosis via its function as an opsonin. Activation of C3 also leads to the formation of a C5-convertase, leading to the assembly of the terminal C5b-C9 complex, otherwise termed the membrane attack complex (MAC). The MAC creates pores in the membrane of the invading pathogen, eventually leading to their cell-lysis and death.