The complement system primarily functions to enhance inflammation and promote the lysis of foreign cells and pathogens through a cascade of protein interactions.

Factor B is a component of the alternative complement pathway, not the classical pathway.

C3 convertase is an enzyme complex that cleaves C3 into C3a and C3b, initiating the formation of the membrane attack complex.

C3b is the complement protein that binds to foreign cell surfaces, marking them for phagocytosis by immune cells.

The membrane attack complex (MAC) forms pores in the cell membrane of foreign cells, causing cell lysis and destruction.

C1 inhibitor is a regulatory protein that controls the classical complement pathway by inhibiting the activity of C1, preventing excessive activation.

C5a is a complement protein that activates neutrophils and macrophages, promoting inflammation and enhancing phagocytosis.

C4b, along with C2a, forms the C5 convertase complex, which cleaves C5 into C5a and C5b.

Properdin is a protein that stabilizes the C3 convertase complex in the alternative complement pathway, enhancing its activity and promoting complement activation.

C5 is the complement protein that undergoes cleavage to generate anaphylatoxins, including C3a and C5a, which have various inflammatory and immune-modulating effects.

C3aR and C5aR are receptors for C3a and C5a, respectively. When activated, these receptors trigger various responses, including the activation of neutrophils and macrophages, promoting inflammation and phagocytosis.

C5b is the complement protein that initiates the assembly of the membrane attack complex (MAC) by binding to C6 and subsequent complement proteins, leading to the formation of pores in the cell membrane.

Factor D is a serine protease that activates C3 convertase in the alternative complement pathway, leading to the cleavage of C3 into C3a and C3b.

The C3 convertase complex in the classical complement pathway is formed by the binding of C4b to C2a, leading to the cleavage of C3 into C3a and C3b.

C4bp (C4 binding protein) is a regulatory protein that inhibits the alternative complement pathway by binding to C4b and preventing its interaction with C2a, thereby preventing the formation of C3 convertase.