Answer:
One way in which complement activation destroys pathogens is by C3b binding to the surface of microbes, which then causes inflammation through histamine and heparin release.
Explanation:
C3b binds to the surface of microbes (opsonin), and functions as a component of C3 and C5 convertases while C3a stimulates inflammation.
The alternative pathway of complement activation is triggered by the deposition of C3b on the surface of a microbe. The microbe- bound C3b binds another protein called Factor B, which is then broken down by a plasma protease called Factor D to generate the Bb fragment.
This fragment remains attached to C3b, and the C3bBb complex functions as an enzyme, called C3 convertase, to break down more C3. The C3 convertase is stabilized by properdin, a positive regulator of the complement system.
As a result of this enzymatic activity, many more C3b and C3bBb molecules are produced and become attached to the microbe. Some of the C3bBb molecules bind an additional C3b molecule, and the resulting C3bBb3b complexes function as C5 convertases, to break down the complement protein C5 and initiate the late steps of complement activation.
The main effectors of the complement system are opsonization, cell lysis and inflammation. It also stimulates B cell responses and antibody production.
