When antigens enter into the body, normallythis antigen will be recognized by the antibody that has been generated beforeduring first exposure. The antibody binds to the soluble antigen forming theantibody-antigen complexes in the circulation in order to clear up all of thepathogens. According to Levinson (n.
d), the reticuloendothelial system ormacrophages system and other phagocytes have the ability to remove the immuneantibody-antigen complexes very effectively in a normal condition. However, in typeIII hypersensitivity, these systems are not capable to remove these complexes.As a result, this antigen-antibody complexes tends to deposit on the wall of theblood vessels. Some of the immune complex deposition on the blood vessel willactivate the complement protein such as C1, C4, C3 and C5-9 resultingmembrane attack complex, leukocytes chemotaxis, leukocytes polymorphism andphagocytosis as well as inflammation. So that, in classical pathway C1 binds tothe antigen-antibody complex and become activated C1.
Robbins, Kumar and Cotran(2013) stated that the activated C1will activate C4 and C2 resulting C3convertase. This C3 convertase play a vital role as it will activate the thirdcomponent of complement system which is C3 component and this C3 component isfurther cleaved by C3 convertase into C3a and C3b. Then binding of the C3b tothe C3 convertase will result the formation of the C5 convertase and this C5convertase able to split C5 complement protein leading to formation of C5a andC5b. This C5b will bind to C6-9 resulting membrane attack complex that iscapable to make a hole in the membranes of invading microbes leading to lysisof the microbes ( Robbins, Kumar and Cotran, 2013, pg46-47 ). This mechanism isillustrated in the picture 1.
However,C5a and C3a that are formed and released can attract the neutrophils andactivate mast cell degranulation. C5 complement system plays a chemotacticagent by attracting the neutrophils and this neutrophil can produce the enzyme thatcould damage the endothelial cells of the blood vessels resulting release ofthe red blood cell from the blood vessels. This can be proven by Robbins, Kumarand Cotran (2013) who stated that, activation of the leukocytes at theantibody-antigen complex deposition result the production and release of thelysosomal enzyme and reactive oxygen species. These kinds of substances canlead to the adjacent tissue injuries.
On top of that, C5a and C3a also act asanaphylatoxin substances which could cause mast cell degranulation. The extremeneutrophil action and mast cell degranulation causes Type III hypersensitivity.