Pathogens manipulate the complement system in diverse ways, inhibiting immune attack or exploiting its components for survival. Strategies include decoy molecules, cleavage and inactivation of complement proteins, and recruitment of host regulators. Pathogens may mimic host cells to evade detection or use complement components as a nutrient source. This dynamic interplay showcases the complexity of host-pathogen interactions.

The complement system is vital for fighting pathogens but must be regulated to avoid harmful consequences like tissue damage, autoimmunity, and inflammation. Components like CR1, CD55, CD46, Factor H, and CD59 play key roles in regulating complement activation, preventing uncontrolled responses and maintaining effective immune defense without harming host tissues.

The membrane attack complex (MAC) forms in the complement cascade after C3 activation. The process involves C3 convertase formation, C3b binding to pathogen surfaces, C5 convertase assembly, and C5 cleavage. MAC assembly includes C5b, C6, C7, C8, and multiple C9, creating a transmembrane channel leading to cell lysis and pathogen destruction.