The complement system consists of 11 special proteins (designated C1-C11) that supplement or complement the action of antibodies. The complement system has two different pathways – classical and alternative. The classical system is the more rapid of the two pathways.
Classical pathway
Imagine a team of navy seals executing maneuvers to plant charges on the hull of a marked enemy ship. C1 is a bit like one of those seals; it binds to antibody that is bound to antigen (antigen-antibody [Ag-Ab] complex) on the target cell surface.
The Ag-Ab complex catalyzes a series of chemical reactions that ends with inactive C3 converting to its active form, C3b, which then binds to the surface of the target antigen.
Once bound, C3b stimulates phagocytosis and promotes inflammation. C3b also triggers reactions that lead to the creation of a membrane attack complex (MAC) that creates pores in the membrane of the target cell, like holes blown in the hull of a ship.
When the target is not marked (no Ag-Ab complex), the navy divers do not know where the enemy ship is, so other techniques (alternate pathway) are used to detect and mark the location of the enemy ships. The alternative pathway uses communication satellites (complement proteins) suspended in the plasma that become activated on contact with foreign materials.
The activated proteins catalyze a series of reactions that result in conversion of C3 to C3b, stimulation of phagocytosis, and formation of membrane attack complex (explosives planted by the navy seals). Proteins of the alternative pathway interact in the plasma in response to contact with bacteria, certain parasites and virus-infected cells. However, the alternate pathway results in an overall slower response, because the alternate pathway functions to trigger the classical pathway, which then destroys the target.
In addition to destroying foreign invaders, complement causes degranulation of mast cells, and formation of the membrane attack complex – a group of lipid-soluble proteins that punch holes in the cell membrane of pathogens.
Degranulation of mast cells and basophils results in the release of histamine, which initiates the inflammatory response. Histamine is one of a number of chemical messengers (cytokines) involved in immune response. Other cytokines include interleukins, interferons, tumor necrosis factors, chemicals that regulate phagocytic activity, and colony-stimulating factors that stimulate blood cell production in bone marrow and lymph tissues.
Histamine attracts more leukocytes to the area, and opens pores in capillaries to allow plasma proteins and fluid to pass into the interstitial space causing edema. Histamine also dilates blood vessels increasing blood flow to the area. The result is inflammation.
Foreign and abnormal antigens trigger lymphocyte production and stimulate lymphocytes to produce antibodies in response. Once an invader has been recognized, more antibodies are made to attack and neutralize it. When antibodies identify and bind antigens, phagocytes engulf the resulting Ag-Ab complex, and neutralize or disassemble them.
