When antigens enter into the body, normally this antigen will be recognized by the antibody that has been generated before during first exposure. The antibody binds to the soluble antigen forming the antibody-antigen complexes in the circulation in order to clear up all of the pathogens. According to Levinson (n.d), the reticuloendothelial system or macrophages system and other phagocytes have the ability to remove the immune antibody-antigen complexes very effectively in a normal condition. However, in type III hypersensitivity, these systems are not capable to remove these complexes. As a result, this antigen-antibody complexes tends to deposit on the wall of the blood vessels. Some of the immune complex deposition on the blood vessel will activate the complement protein such as C1, C4, C3 and C5-9 resulting membrane attack complex, leukocytes chemotaxis, leukocytes polymorphism and phagocytosis as well as inflammation. So that, in classical pathway C1 binds to the antigen-antibody complex and become activated C1. The activated C1will activate C4 and C2 resulting C3 convertase. This C3 convertase play a vital role as it will activate the third component of complement system which is C3 component and this C3 component is further cleaved by C3 convertase into C3a and C3b. Then binding of the C3b to the C3 convertase will result the formation of the C5 convertase and this C5 convertase able to split C5 complement protein leading to formation of C5a and C5b. This C5b will bind to C6-9 resulting membrane attack complex that is capable to make a hole in the membranes of invading microbes leading to lysis of the microbes ( Robbins, Kumar and Cotran, 2013, pg46-47 ). This mechanism is illustrated in the picture 1. However, C5a and C3a that are formed and released can attract the neutrophils and activate mast cell degranulation. C5 complement system plays a chemotactic agent by attracting the neutrophils and this neutrophil can produce the enzyme that could damage the endothelial cells of the blood vessels resulting release of the red blood cell from the blood vessels. This can be proven by Robbins, Kumar and Cotran (2013) who stated that, activation of the leukocytes at the antibody-antigen complex deposition result the production and release of the lysosomal enzyme and reactive oxygen species. These kinds of substances can lead to the adjacent tissue injuries. On top of that, C5a and C3a also act as anaphylatoxin substances which could cause mast cell degranulation. The extreme neutrophil action and mast cell degranulation causes Type III hypersensitivity.