Final answer:
Endogenous complement can be inactivated by regulatory proteins that prevent the complement complex from damaging host cells. Mutations affecting the binding of complement proteins can compromise the effectiveness of the complement system even if the system still partially functions.
Step-by-step explanation:
Endogenous complement proteins can be inactivated through the action of endogenous regulatory proteins, which protect host cells from accidental damage by the complement system. These regulatory proteins ensure that the complement cascade is directed only against pathogens, preventing the complement complex from adhering to and damaging the cells of the organism producing them. If a series of genetic mutations occurred that hindered some, but not all, of the complement proteins from binding antibodies or pathogens, the overall function of the complement system could still be affected, as the system operates through a highly coordinated and sequential cascade. The removal or alteration of even a few proteins in this cascade can lead to a reduced capacity to fight infections, though the extent of this reduction would depend on which and how many components were affected.
The complement system involves both the classical pathway, which requires antibody binding, and alternative pathways that do not. Both pathways ultimately lead to the destruction of pathogens through a series of steps including opsonization (marking pathogens for destruction by phagocytes), triggering inflammation, and the formation of membrane attack complexes that lyse the pathogen.