The complement system involves complement proteins labelled C1-C9. It involves a series of reactions that happen along the membrane of a pathogenic cell ultimately resulting in the destruction of that cell.
The complement system can work on its own to generate inflammation and destroy pathogens (via the lectin and alternative pathways).
It also forms a key way in which antibodies can generate inflammation and lead to pathogen destruction (via the classical pathway).
Triggers
- Classical Pathway
- Activated by antibody-antigen complexes binding to C1 (this is called complement fixation)
- Lectin Pathway
- Activated when mannose binding protein binds to mannose on pathogens, which then binds to MBL-associated serum protease (MASP) which then activates the pathway.
- Alternative Pathway
- C3 is spontaneously activated along cell membranes.
- In membranes of normal cells there are proteins that deactivate the pathway.
- In pathogens without the regulatory process the pathway remains activated.
Outcomes
- C3b is created which acts as an opsonin for phagocytosis of the attached cell.
- C5a is created which attracts cells to the site of inflammation (neutrophils, monocytes and eosinophils).
- C3a, C4a and C5a activate mast cell degranulation.
- C3a and C5a activate eosinophil degranulation.
- Membrane Attack Complex (C5b678) is a large molecule that enter cell membranes and creates a hole that leads to cell lysis. C9 molecules can be added to this complex to make the hole in the cell membrane larger.